New Genetics and Society
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Epigenetics for the social sciences: justice,
embodiment, and inheritance in the postgenomic
age
Maurizio Meloni
To cite this article: Maurizio Meloni (2015) Epigenetics for the social sciences: justice,
embodiment, and inheritance in the postgenomic age, New Genetics and Society, 34:2,
125-151, DOI: 10.1080/14636778.2015.1034850
To link to this article: http://dx.doi.org/10.1080/14636778.2015.1034850
Published online: 12 May 2015.
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Date: 12 July 2016, At: 12:57
New Genetics and Society, 2015
Vol. 34, No. 2, 125 –151, http://dx.doi.org/10.1080/14636778.2015.1034850
Epigenetics for the social sciences: justice, embodiment,
and inheritance in the postgenomic age
Maurizio Meloni∗
Institute for Advanced Study, School of Social Science, Princeton, USA
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(Received 11 May 2014; final version received 10 December 2014)
In this paper, I firstly situate the current rise of interest in epigenetics in the
broader history of attempts to go “beyond the gene” in twentieth-century
biology. In the second part, after a summary of the main differences between
epigenetic and genetic mutations, I consider what kind of implications the sui
generis features of epigenetic mutations may have for the social sciences. I
focus in particular on two sites of investigation: (a) the blurring of the
boundaries between natural and social inequalities in theories of justice and
their possible implications for public policy and public health and (b) a
deepening of the notion that the constitution of the body is deeply dependent
on its material and socially shaped surroundings (“embodied constructivism”).
In conclusion, I advance some cautionary reflections on some of the (known
and unprecedented) problems that the circulation of epigenetics in wider
society may present.
Keywords: epigenetics; natural/social inequalities; public health implications
Introduction
Epigenetics represents one of the key terms with which to grasp the profile of the
new biological landscape that has taken shape in the so-called postgenomic age
(so-called because it is conventionally used to define the period dating after the
completion of the Human Genome Project in 2003). Of this postgenomic age,
with its tensions and promises, hypes and controversies, epigenetics is a perfect
incarnation and an excellent theoretical spyglass through which to see the changing
thought-style (and possibly ethos) of the biosciences in this early twenty-first
century.
Epigenetics was originally conceived by embryologist Conrad H. Waddington
(1905 – 1975; see Slack 2002) as the investigation of the unfolding of genetic
material into a final phenotype (1942; see Holliday 1990, 2006). Today, it is
increasingly understood in a molecular sense, as “the study of changes in gene
function that are mitotically and/or meiotically heritable and that do not entail a
∗
Emails: [email protected], [email protected]
# 2015 Taylor & Francis
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126
M. Meloni
change in the sequence of DNA” (Armstrong 2014). In the context of a postgenomic proliferation of – omics studies (genome, microbiome, transcriptome, exposome, etc.) – epigenetics’ contribution is the study of the epigenome, the set of the
potentially “heritable changes in gene expressions that occur in the absence of
changes to the DNA sequence itself” (Dolinoy and Jirtle 2008).
In this article, I have a threefold goal. First, I situate the last decade’s
explosion of interest in epigenetics within a broader perspective that takes in
the tensions and persisting challenges to notions of hard-heredity in the history
of biology, and genetics in particular. Second, I investigate some of the possible
implications of epigenetics for social science and wider society. I will look in
particular at two ossified conceptual dichotomies in political and social theory
that are likely to be challenged by the rise of epigenetics: (a) the boundary
between natural and social inequalities in theories of justice and (b) the opposition between biomedical and social constructionist views of the body. Finally, I
will address some of the counterintuitive implications that claims of a replacement of hard-heredity (heritable material impervious to direct environmental
influences) with an epigenetic or soft view of inheritance (heredity is malleable,
modulated by direct environmental variations) may have on public policy and
public health.
The context: from the crisis of the gene to the “reactive genome”
The quest for mechanisms of nongenetic inheritance is far from new in the history
of biology. Repeated attempts to go “beyond the gene” (Sonneborn 1949; Sapp
1987) and search for extrachromosomal forms of inheritance (Harwood 1993)
have characterized twentieth-century biology more than textbook histories of
biology allows to think. Far from being an ideological return to Lysenko, as polemically claimed (Maderspacher 2010), the current rise of interest in the mechanisms
of epigenetic inheritance can be better seen as the last symptom of a longer term
crisis in the notion of the gene with important implications for modern evolutionary
theory and a remaking of the notion of heredity.
Postgenomic genome
A crisis in the notion of the gene is nothing new. The gene has always been a
concept in “tension” (Falk 2003), situated in a complex history of experimental,
technological, and conceptual settings (Beurton et al. 2003; Rheinberger and
Müller-Wille 2010). However, what has happened after the completion of the
Human Genome Project has made this crisis even more conspicuous.
To paraphrase Portin (2002, 274), our current postgenomic understanding has
outgrown conventional knowledge of the gene. In a postgenomic context, where
it is becoming harder to maintain a realist and particulate notion of the gene
(Barnes and Dupré 2008), what is increasingly brought to light is the reactivity
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New Genetics and Society 127
of the new postgenomic genome to environmental signals (Keller 2012, 2014; see
also Gilbert 2003; Griffiths and Stotz 2013). The genome is best described today as
a “vast reactive system” (Keller 2012), a mechanism “for regulating the production
of specific proteins in response to the constantly changing signals it receives from
its environment” (Keller 2014, 2427).
This shift in focus from the centrality of DNA to its broader regulatory (cellular
and environmental) context may open the way to a different view of evolution and
inheritance. Whereas the “transmission genetics” model (Mameli 2005; Amundson
2005) saw heredity merely as the simple passage of DNA from one generation to
another (see also: Müller-Wille and Rheinberger 2012), we are today increasingly
encouraged to look at the fact that “heredity involves more than DNA”, and that
variations arising during development may be inherited (Jablonka and Lamb
2008). The same so-called central dogma of molecular biology, which states the
unidirectional nature of the flow of information from DNA to protein (Crick
1970), is increasingly challenged on the ground that information can also go in
the reverse direction (Dupré 2012). It is in this turbulent intellectual context that
the current wave of interest in epigenetics has to be situated (Jablonka and Raz
2009).
Enter epigenetics
Bases and mechanisms
To understand epigenetics, it is a good idea to start from the biochemical bases of
the process, namely the fact that, in eukaryotic cells, DNA is tightly wrapped into
chromatin and that modifications of the chromatin structure can affect DNA
expression (Meaney and Szyf 2005; Feil and Fraga 2012).
DNA methylation (the most recognized mechanism of epigenetic mutations, and
studied since the late 1960s, see Holliday 2006, see however Daxinger and Whitelaw 2012) is one such change by which the attachment of a methyl group to a DNA
base results in chromatin de-activation and inhibition of gene transcription. Methylation works therefore as a sort of “physical barrier to transcription factors” (Gluckman et al. 2011) and is regulated by nutritional and environmental factors,
especially during phases of early development (Dolinoy and Jirtle 2008).
Further epigenetic mechanisms include histone modification and regulation by
non-coding RNA, although they are considered less stable than methylation
patterns.
There are several excellent examples of very visible phenotypic changes in the
animal kingdom driven by changes in methylation patterns as a result of different
environmental exposures and nutritional inputs. For instance, in honeybees (Apis
mellifera), genetically identical larvae following differential feeding (royal jelly
versus less rich food) produce alternative adult phenotypic (sterile worker and
fertile queen: Kucharski et al. 2008).
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128 M. Meloni
In experimental contexts, the most well-known case of nutritional control of
alternative phenotypic outcomes is probably the switching on and off of the
agouti gene in mice that is obtained by feeding a rich in methyl-donor diet to pregnant agouti mice. Exposing the pregnant mouse to lack of methyl-rich donor diet
results into hypomethylation (and enhanced expression) of the promoter of the
agouti gene. This brings to highly visible phenotypic changes because offspring
are no longer slim and brown, but yellow, fat, and prone to diabetes (Waterland
and Jirtle 2003).
If we move from nutritional to behavioral exposures, the most well-known case
is Meaney’s group study on how high versus low licking and grooming behaviors
in rats alter the methylation patterns of the promoter of the glucocorticoid receptor
in pups (Weaver et al. 2004; see an updated review in Lutz and Turecki 2014).
The most hotly debated issue in epigenetics concern probably the stability and
evolutionary significance of transgenerational epigenetic inheritance (Richards
2006; Jablonka and Raz 2009; Daxinger and Whitelaw 2010, 2012; Grossniklaus
et al. 2013; Lim and Brunet 2013; Heard and Martienssen 2014). To clarify
what is at stake here, it is important to distinguish two alternative, but often confused, aspects that go under the label of epigenetic transgenerational effects: (a)
germ line inheritance (where the epigenetic signature is not entirely cleared in
gametogenesis and can be transmitted through the germ line: Chong and Whitelaw
2004; see Anway et al. 2005) and (b) non-germ line, experience-dependent epigenetic inheritance (where the epigenetic signature is re-established in each successive generation by the reoccurrence of the “behaviour or environment that
induces the mark”, also known as “niche recreation”: Gluckman et al. 2011) as
in the case of the Meaney’s group studies above mentioned.
The possibility of transgenerational epigenetics phenomena in humans remains
very controversial. There are very well-known epidemiological studies on the
transgenerational effects of chronic disease in individuals prenatally exposed to
famine during the Dutch Hongerwinter (Hunger Winter) in 1944 –1945 during
German occupation (Heijmans et al. 2008; Painter et al. 2008), as well as studies
on the link between ancestors’ access to food and longevity drawn from the historical record of the Overkalix cohorts in Northern Sweden (Bygren, Kaati, and
Edvinsson 2001).1 These studies establish connections between malnutrition in
utero and in early life, and persisting metabolic disorders (up to six decades later
that is including the second generation, Painter et al. 2008) via changes in the
human epigenome.
The debate, however, on the mechanisms, significance, and magnitude of these
transgenerational2 effects remains very much open, given the fact that the erasure
of methylation marks between generations is what is in principle to be expected in
mammalian development (although not a universal phenomenon in other organisms,
and not complete even in mammals, see Richards 2006, and Lim and Brunet 2013, on
“unconventional modes of inheritance”).3 Cautiousness is certainly necessary, as
scientists remind us that there is still a “long way to go” to fully understand “the
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involvement of epigenetics in environmentally triggered phenotypes and diseases”
(Feil and Fraga 2012, 107; see also Heard and Martienssen 2014).
The uniqueness of epigenetic mutations
Scientific controversies and hype undoubtedly surround epigenetic research
(Meloni and Testa 2014). Speculation on such a scientifically unstable field may
be seen as premature. However, recognition of exaggerated claims and controversial issues is not a sufficient reason to shy away from the potential of epigenetic
research, especially when understood in sophisticated postgenomic frameworks.
My argument is that what we already know about epigenetics and the new reactive
view of the genome that is emerging from postgenomics offer us enough conceptual elements to think in a different way the separation of the human world into a
“biological” and a “social” domain that was characteristics of the century of the
gene (and a reflex of its hard-hereditarian framework). Before assessing some of
the distinctive implications of epigenetics for the social sciences, it is important
to recap the uniqueness displayed by epigenetic mechanisms when compared to
genetic ones.
As the following table indicates (elaborating on Jablonka and Lamb 1995; Rando
and Verstrepen 2007; Loi, Del Savio, and Stupka 2013; Landecker and Panofsky
2013), the crucial differences between epigenetic and genetic mutations can be
summed up in seven dimensions:
Epigenetic mutations
(1) Sensitivity to the environment in short social
time span
Epigenetics as a mechanism for flexible and
dynamic responses to the solicitations from a
changing environment
Directed variation as a consequence of a
“specific environmental agent inducing
specific and predictable heritable changes”
(Jablonka and Lamb 1995)
The randomness of epigenetic variations is
questioned (Jablonka and Lamb 2005; Rando
and Verstrepen 2007). Non-random, although
not necessarily adaptive responses (Jablonka
and Lamb 1995)
(2) Potential reversibility through practice,
lifestyle or therapy (e.g. pharmacological
intervention) and other post hoc interventions
(Szyf 2009)
Genetic mutations
(1) Unresponsive to direct environmental signals
(with exceptions of accidental effects, such as
mutations due to exposure to X-rays, nuclear
radiations, etc.)
Random mutations: “independent of selective
pressure” (Rando and Verstrepen 2007); only
due “to the imperfections of the copy-system
or to non-directed effects of environmental
factors” (Jablonka and Lamb 1995)
(2) Not affected by lifestyle in “short” social time,
only over a long evolutionary timescale (e.g.
gene-culture coevolution: lactase persistence
in specific human populations with increased
nutrition from dairy)
130 M. Meloni
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(3) Early programming
In utero or perinatal events set stably epigenetic
marks
Embedding of early-life experiences and earlylife environment in the genome via epigenetic
mechanisms (Champagne and Curley 2009;
Szyf and Bick 2013)
Genome-wide effects of epigenetic responses to
early-life adversity (McGowan et al. 2011)
(4) Short-term adaptive flexibility
Stable enough to allow intergenerational
transmissibility over a certain (limited)
number of generations
Many ecological challenges are too transient to
be “dealt with effectively by changes in gene
frequencies”, but “too chronic to be efficiently
buffered by homeostasis or allostasis”: hence,
importance of an epigenetic adjustment to
variable environmental and behavioral
experiences (Kuzawa and Bragg 2012; see
Jablonka and Raz 2009)
(5) Tissue and cell specificity (different
epigenetic marks depending on different cells)
One body many epigenomes (Wade 2009)
(6) Time dependency: epigenetic marks will
change depending on the time a sample is
taken
Age-related changes
(7) Unit of inheritance: broad
The whole cellular architecture, or gene’s
phenotype (Jablonka and Lamb 1995)
including DNA, chromatin structure, etc.
(3) Insensitive to in utero or post-natal events
(with the exceptions of events indicated in 1)
No link between early-life events and genetic
sequences
(4) Long-term adaptive flexibility
Inherited features acting only over long
evolutionary timescale/countless generations
Thousands of years before fixing a change in the
genetic pool
(5) One body one genome (although this is
increasingly challenged: chimerism,
mosaicism, see Dupré 2012, Chap. 7)
(6) One-time DNA sample invariant for life
No change of DNA during life
(7) Unit of inheritance: narrow
The nucleotide sequence
It is building upon this specificity and singularity of epigenetic phenomena that it
is possible to anticipate some of the possible reconfigurations of the relationship
between the biological and the social in a postgenomic scenario.
A significant body of scholarship has already started to outline the implications
of these anticipated differences between the specific features of this nongenetic
pathway of inheritance vis-à-vis a genetic one. Many of the points in the table
have already received a significant level of attention in social science investigation.
Issues of extended personal, social, and legal responsibility arise from points 1–2
(Rothstein, Cai, and Marchant 2009; Dupras, Ravitsky, and Williams-Jones 2014;
Hedlund 2012). Increasing attention and intervention on the maternal body are an
effect of point 3 which clearly situates mothers and their behaviors at the center of
epigenetic attention (Richardson, forthcoming; Richardson et al. 2014), often interlaced with racial themes (Mansfield 2012). Risk of classifying sub-populations with
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different epigenetic marks because of the reproduction/perpetuation of hard social
conditions (Katz 2013 ; Meloni 2014; Meloni and Testa 2014) is a consequence of
point 4. And the issue of a new class of sensitive information in need of privacy
protection arises from point 5 (Rothstein, Cai, and Marchant 2009).
In the second part of this article, I will therefore direct my attention to two other
possible implications of epigenetic research for social and political science, which
have received relatively less attention so far. In conclusion, I will raise a prudent
warning about some unforeseen implications that the circulation of epigenetics
in wider society may present.
Epigenetics and political theory: blurring the boundaries between natural
and social inequalities
How much is genetic luck really due to luck?
The first area in which I would like to measure the social implications of epigenetics
research may seem speculative, but has important implications in the way notions
of inequalities and theories of justice are constructed.
Differences between “natural” and “non-natural” features of human experience
are amongst the most deeply rooted assumptions in Western metaphysics. This
dichotomy has been visible since Antiquity in both medical thinking (Galen) and
theories of justice (Plato, Aristotle). In both fields, the separation between
“natural” and “not natural” plays the same powerful function to distinguishing
what is within human control and what is outside it.
In medical thinking, categories like “naturals” and “non-naturals” were still
influential until early modernity to mark the boundaries between non-mutable
and modifiable aspects of human life: temperament and constitution for the first,
nutrition, and climate for the latter (Beltran 2002; Müller-Wille and Rheinberger
2012).
In socio-political thought, we see at stake a similar dichotomy (Beteille 1983;
Lewens 2010). In Plato and Aristotle, notions of natural inequalities perform a
key function in sustaining a stratified view of society. From its classical origin,
the notion of natural inequality represents what lies outside the domain of justice
and human intervention. If an inequality is rooted in nature, there is less (or no)
reason to intervene. In various forms, such a way of thinking has persisted until
the twentieth century, with very few exceptions. Theologically oriented traditions
in political theory that have built the conception of nature upon notions of deity
have further performed this function (Daston and Vidal 2007).
What is particularly striking is that this idea of a state of nature as radically prior
to, and uncontaminated by, social relationships has found a novel legitimation in
modernity through the incorporation of biological arguments into public affairs.
Talks of innate, natural or congenital differences between races, classes, or
genders stemming from biological thinking have re-legitimized ideas of natural
inequalities in politics (Beteille 1983).
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132 M. Meloni
In particular, political theorists in the twentieth century have referred explicitly to
genetics to provide an example of something that is separated or prior to the political domain. Genetics has been often taken as a perfect case of a diverse distribution of talents (the so-called genetic lottery) on which justice has no reason to
intervene or, at the very least, morality rather than justice can be invoked to
justify some sort of rectification. In large areas of political theory, with the exception probably of some egalitarian or consequentialist thinkers,4 genetic disadvantage is seen as a natural asset whose unfortunate effects can be mitigated or
neutralized in a decent society but on which there is no obligation to intervene.
The bottom line argument in much political philosophy seems to be, as Lewens
writes in an insightful article that when, as in the case of genetics, “inequality is
nobody’s fault, it is not the concern of justice to correct it” (2010, 265). As Buchanan and colleagues have remarked, conventional thought in political theory is that:
nature, or the natural, is often thought to be not only that which is given but also that
which must be accepted as beyond human control. In that sense, to say that something is due to nature is to relegate that to the realm of fortune or misfortune,
rather than justice or injustice. ( . . . ) It is not surprising, then, that to a large extent
traditional thinking about justice has associated natural disadvantages with misfortune rather than injustice, since there was little or nothing that could be done to
prevent them. (2000, 83, my italics)
Tom Nagel’s classical article on Nature and Justice is very representative of this
way of thinking for which society has to be seen as less “accountable for those
inequalities in whose generation nature plays a central role” (1997, 305; Lewens
2010). It is not by chance that Nagel picks as a key example a degenerative
illness produced by a defective gene to make the argument for the different
weight that should be assigned to social and natural inequalities, that is, to make
a distinction between injustice and bad luck (or “natural unfairness”). What
Nagel hints at are spheres of human life that “have nothing to do with justice,
and that are not mandatory in the same way” (1997, 303): genetics would be one
of these cases.
Nagel may represent here a particularly conspicuous example of this social/
natural distinction. However, he is not the only one to take this distinction as significant. In Rawls for instance, such a dichotomy between the natural and social is
also taken for granted. As he famously wrote in A Theory of Justice, “The natural
distribution is neither just nor unjust” (Rawls 1971, 87). His semi-consequentialism
implies that “natural primary goods, such as ‘health and vigour, intelligence and
imagination’, fall outside the master patterns by which feasible alternative basic
structures are assessed” (Pogge 1989, 64; Lewens 2010). More recently, in
another very influential article, Anderson (1999, 331) claims that the “distribution
of natural assets” has to be seen out of a “democratic equality” framework. Only the
response of institutions to this distribution, she believes, is politically relevant, but
natural assets are not as such socialized. And many other examples could be given.
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What shall we do with the idea of natural inequalities in an epigenetic age?
Over the last decades, philosophers of biology have convincingly illustrated the
conceptual confusion of the innate/acquired distinction (Griffiths 2002). In the
light of a developmentalist view of biology and genetics, it is easy for them to
argue against any neat distinction between the “effects of natural differences
from effects of social differences” (Lewens 2010, 271).
The first argument I want to make here, expanding in particular on an important
article by Loi, Del Savio, and Stupka (2013), is that epigenetics makes the inappropriateness of the natural/social divide for political theory highlighted by Lewens
even more flagrant. Epigenetics provides “a chain of connections” (Loi, Del
Savio, and Stupka 2013, 143) between what we used to think of separately as
“social” and “natural” inequalities, radically cutting across the distinction
between these two domains. From what we have said in the first part of the
article, epigenetics seems to point to the existence of a double social opening in
the architecture of the gene. Upstream, genetic expression is regulated by the incorporation of certain environmental exposures; downstream, genetic expression can
be reversed via social and pharmacological intervention (Szyf 2009). This
double hole in the structure of the gene calls radically into question the leakproof separation of the “genetics” from the “social” and, accordingly, the equation
of genetics with a natural lottery.
Identifying genetics with a lottery implies understanding it as operating blindly
and immune from the distortions of social structures. The notion of a lottery implies
the idea of a game of chance (Buchanan et al. 2000, 83), a matter of mere misfortune upon which no call for responsibility can be made. In abstract, being born with
a faulty gene (Nagel’s case) may be thought of as just poor chance.
The idea of a genetic lottery fits well with the twentieth-century view of heredity
as a mere transmission of DNA sequence. However, things become more complicated in epigenetic scenarios when we include in heredity not only DNA sequence
but also how these sequences are expressed. If we take seriously, as epigeneticists
claim, the possibility that genetic expression may incorporate our early life experiences or even the experiences of our ancestors, the picture of the relationship
between the social and the natural, misfortune and choice, appears to change significantly. How much of a role can be given to “poor chance” in cases like the
Dutch Hunger Winter, in which biological disadvantage of two generations is
seen as a direct consequence of the social hardship suffered in 1944? And in
other scenarios where smoking, alcohol, styles of nurturing, or various psychosocial factors seem to directly affect the well-being of present and future generations?
The implications of these studies for public health are clearly far-reaching. Novel
interesting studies inspired by a developmentalist and epigenetic approach have
already started to elaborate a model by which social conditions and material contexts experienced by past generations may become biologically embedded and
somatically transmitted in specific social groups. In these novel models, social
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134 M. Meloni
factors such as nutrition, health care, financial and social capital, education and
public policies in general are embodied and transmitted transgenerationally, thus
perpetuating disadvantaged situations (see the “maternal fitness model”, Wells
2007, 2010; and the “intergenerational phenotypic inertia model”, for instance:
Kuzawa and Sweet 2009).
These studies highlight that neat boundaries between what is “given in nature”,
and therefore not subject to the demands of justice (for instance genetic malfunctioning), and what is instead “socially transmitted” (the long-term effects of
unjust social structures), appear very precarious to maintain. To the extent that
the social operates via the biological and vice versa, chance and choice tend
increasingly to overlap.
This is why epigenetics has the potential to represent an interesting problematization for theories of justice (Loi, Del Savio, and Stupka 2013). Where should a
political demand for justice stop if these epigenetic findings will be further confirmed? And where are the boundaries between personal and collective responsibility in a context where social factors seem so massively engaged in producing
aspects of our own individual biology?
Of course, it is not my goal here to adjudicate between different approaches to
theories of justice. Different political philosophers will look in different ways at
the potential implications of epigenetics. Epigenetics will probably not be a significant change for the two opposite positions of radical libertarians and luck egalitarians (justice as equality of fortune). For the first, no matter the social or natural
origins of an inequality, everyone will be entitled to her/his own lottery ticket
received at birth. For the latter, arbitrary (unchosen) original conditions, be them
natural or social, have to be corrected, so the “faulty gene” of traditional genetic
explanation would be no different from an abnormal methylation pattern caused
by (or, associated with) “unjust” social structure.5
However, leaving these two positions aside, for the remaining arc of socio-political theories, taking epigenetics seriously will have important implications,
although the nature of those implications may be less unidirectional than many
have noticed so far.
Loading the genetic dices?
To reiterate the argument: if genetics is a lottery, from an epigenetic point of view,
“the dice are loaded in the womb” (Gardner 2012). Arguments à la Nagel about a
defective gene’s effects being out of the scope of social justice will be assessed
carefully. At least a second look will be required to adjudicate whether there is a
sense in which previous unjust social situations may have had an influence in
abnormal genetic functioning.
More importantly, because of its supposed protection from the distortion of
social structures, the notion of a genetic lottery still possesses a democratic and
egalitarian allure in the eyes of many political philosophers. This argument has
New Genetics and Society 135
a long tradition in biology (firstly in Weismann 1891), and was remade in the last
two decades by Francis Fukuyama, when he claimed that far from being “inherently unfair” “because it condemns certain people to lesser intelligence, or bad
looks, or disabilities of one sort or another”, the genetic lottery is actually:
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profoundly egalitarian, since everyone, regardless of social class, race or ethnicity,
has to play in it. The wealthiest man can and often does have a good-for-nothing
son ( . . . ) the genetic lottery guarantees that the son or daughter of a rich and successful parent will not necessarily inherit the talent and abilities that created conditions
conducive to the parents’ success. (2002, 156)6
My argument is that this democratic allure of genetics will be easily lost if epigenetics prevails. Epigenetic findings undermine Fukuyama’s view that the genetic
lottery is inherently impartial and blind. In an epigenetic view, the genetic lottery
(genetic transmission + genetic expression) is always influenced by the social disparities of the past, from individual behaviors (smoking, etc.) to social processes
(war, poverty, injustice, etc.).
If genes have their own biological memory, the genetic lottery loses its original
veil of ignorance. It brings the mark of a certain social inertia, is no longer impartial, and we cannot fully count on it as a fair referee distributing randomly natural
assets. Such a denaturalization of the genetic lottery has two profound implications.
On one side, it may be used for broadening the scope of theories of justice. In
their seminal book on genetics and justice, Buchanan and colleagues anticipated
a colonization of the natural by notions of justice from the viewpoint of new
genetic technologies making possible a change of human nature (2000). In a different sense, epigenetics may bring a similar colonization of the natural via social
justice. Loi, Del Savio, and Stupka (2013) have argued that a deconstruction of
the natural/social border implies that luck-egalitarian proposals in which there
are no moral differences between unchosen natural and social disadvantages, and
Rawlsian approaches that are limited to social inequalities, will increasingly
come to overlap. To the extent that for instance class inequalities are now seen
to operate via biological endowments, the Rawlsian principle for a fair equality
of opportunity can be broadened to include biological assets (Loi, Del Savio,
and Stupka 2013).
On the other side, however, this translation of epigenetic themes in public policy
and public health debates may be less unidirectional (expanding justice) than this
liberal agenda might like. Here is where some knowledge of the history of biopolitics may help. What has not to be forgotten is that the public health implications of
soft-inheritance are full of problematic and often counterintuitive aspects.
Lamarckism in public policy, of which today epigenetics would be an actualization,
has always been an ambiguous force (Bowler 1984; Meloni, forthcoming). It can be
used to promote social reform because, obviously, investing massively on the social
is not a wasted effort if good habits can be passed on across generations (as “leftLamarckians” like Paul Kammerer highlighted in the 1920s).
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136 M. Meloni
However, the inheritance of acquired characters is a double-edged sword: also
bad habits can become bad biology, and the scars of past exposures and traumas
can give rise to ideas of specific groups being “too damaged7” to be rescued. Inheritance in sum can be “poisoned”, as a recent headline in The Economist (2013) has
significantly claimed, commenting on new epigenetics studies.8 If one looks at the
debate in Europe and America until the 1910s, when soft-hereditarian ideas were
still used in public policy and public health debates, this notion of a poisoned heredity (or a “racial poison”) was widespread and not always employed for progressive goals. For instance, the notion that alcoholism or life in the slums could
irremediably damage not only the germ-plasm of exposed people but also that of
their offspring was quite common at the time. In sum, the sins of the fathers
would leave the new generation in a situation of biological inferiority from the
very beginning. Upon this poisoned heredity, a racism or classism complementary
to but different from its more famous hard-hereditarian version was easily promoted
(Meloni, forthcoming).
Several neo-Darwinians and Mendelians, from Wallace to Haldane and Huxley,
have highlighted over time these problematic aspects of Lamarckian inheritance.
However, the most significant use of this anti-Lamarckian argument in social
policy to my knowledge was made in the 1920s by Soviet geneticist and eugenicist
Yuri Filipchenko when he claimed, in Loren Graham’s words, that if Lamarckism
not Mendelism was true:
all socially or physically deprived groups, races, and classes of people-such as the
proletariat and peasantry and the nonwhite races-would have inherited the debilitating effects of having lived for centuries under deprived conditions. Far from promising rapid social reform, the inheritance of acquired characteristics would mean that
the upper classes are not only socially and economically advantaged, but genetically
privileged as well, a result of centuries of living in a beneficial environment. Thus the
proletariat in Soviet Russia would never be capable of running the state; it was genetically lamed by the inheritance of the effects of its poverty. (1977, my italics; see also
Babkov 2013)
As I will say in my critical final coda, Filipchenko’s argument may still have its
significance today.
The rise of the epigenetic body: how social structures get under the skin
A second contribution of epigenetics to a reformulation of the relationship between
the biological and the social is in the area of theories of embodiment. Since the
1990s, we have witnessed in social theory (Shilling 2003; Williams, Birke, and
Bendelow 2003) and social epidemiology (Krieger 2001a, 2001b, 2004, 2011;
Krieger and Davey Smith 2004) to an increasing recourse to the notion of “embodiment” to undermine the sterile opposition between biomedical models (endogenous causes of disease) on one side, and social constructionist views (body as the
effect of language/power structures), on the other.
New Genetics and Society 137
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As I will highlight next, also in theories of embodiment, epigenetics can significantly contribute to undermine established dichotomies between the “natural” and
the “social”.
Embodiment before embodiment
As social epidemiologists are well aware of, there is a long and oft-forgotten history
(Waitzkin 2005) of how social conditions are literally inscribed into human bodies
and socioeconomic disparities are replicated in the bodily structures of people
affected by these differences (Krieger 2005, 2011). The writings of the French
doctor and economist René Villermé, of cell-biologist Rudolf Virchow, as well
as Friedrich Engels’ classical work on the destructive impact of industrialization
on the physiological and moral life of the working class (1844), can be read as nineteenth-century anticipation of an embodiment paradigm (see extended references in
Krieger and Davey Smith 2004; Waitzkin 2005).
The paradox, however, is that in the twentieth century, such references to the way
class differences are manifest in the visual cues of people (“class physiognomies”:
Laurell, quoted in Krieger 2005), have been rather marginalized in social epidemiological studies (Shaw, Tunstall, and Davey Smith 2003). Such discourse was seen
as too resonant with darker biologistic arguments from Lombrosian psychiatry to
eugenics.
In the last two decades, however, something has started to change again in this
domain. From neuroscience to social epidemiology, it seems possible again to
invoke the physiological and the somatic level in social explanations, without
falling back into classical deterministic arguments. Rather, what is emphasized in
this new wave of studies is the continuous and plastic interchange of the body
with its material surroundings.
The new embodiment
Since the 1990s, cumulative evidence of the impact of social contexts on the human
body has become increasingly available. Data from biomedical and psychoneuroimmunological research have highlighted the dependence of neuroendocrine
and immune functions on social structures and social and psychological processes
(Cacioppo 1994; Cohen and Herbert 1996), and emphasized how social characteristics and structures of neighborhood and communities (Diez Roux, Jacobs, and
Kiefe 2002; Sampson 2003) have a profound impact on well-being and cardiovascular health.
Social relationships, social integration, support, and social networks have been
increasingly linked to longevity, and seen as “intrinsically beneficial” to physical
health (Seeman 1996; Cohen 2004; Brown et al. 2009; Cohen and JanickiDeverts 2009; Kok and Fredrickson 2010). On the other side, social isolation
and rejection, loneliness, and disruption of social networks are increasingly seen
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138 M. Meloni
as major causes for morbidity and mortality (Cacioppo et al. 2002, 2006; Cacioppo
and Patrick 2008; Cacioppo, Hawkley, and Thisted 2010).
Moving from the individual body to the “body economic”, there is now an
increasing number of studies focusing on the way in which austerity policies
and inequalities are literally “killing” factors (Stuckler and Basu 2013; Therborn
2014). These recent works constitute the apex of a longer tradition of social
research on the way in which inequality, discrimination, and racism literally
harm health (Clark et al. 1999; Krieger 2001a, 2001b, 2011, 2004). Probably
the most significant and investigated construct in this area, for its implications
for public health, is socioeconomic status (SES). Since the early 1990s, studies
on SES discovered a strong link between low social status and higher mortality
rates (Marmot et al. 1991). Detailed studies exist today connecting SES to
asthma (Chen et al. 2006), changes in immune responses (Chen et al. 2003;
Dowd and Aiello 2009), increased cardiovascular disease risk factors (particularly
amongst non-Hispanic Blacks: Sharma et al. 2004), abnormal cortisol secretion in
young children (Lupien et al. 2000, 2001), dysregulation of the stress axis and
response (Evans and Kim 2007). In general, the pathways by which SES is
seen to drive disease include systemic inflammation, cellular processes, and
genomic pathways (Chen and Miller 2013; see also Wolfe, Evans, and Seeman
2012).
Finally, in the last decade, neuroscience has gained the lion’s share in this literature on the embodiment of social influences and the effects of SES in particular. At
the core of the recent wave of neuroscientific studies is the growing appreciation for
the plasticity of the brain, including the adult brain (Rosenzweig and Barnes 2003;
Rubin 2009; McEwen and Gianaros 2010). The recognition of plasticity, how the
brain constantly responds to and is literally shaped by environmental contexts,
makes possible to establish increasing connections between social settings and
brain morphology and functions.
Several neuroscience-based studies have addressed directly how SES impacts
not only cognitive and emotional development, but also the volumes of the hippocampus and the amygdala, memory, and certain aspects of executive function,
including cognitive control (respectively: Noble, Norman, and Farah 2005; Farah
et al. 2006; Noble, McCandliss, and Farah 2007; Hackman and Farah 2009;
Hackman, Farah, and Meaney 2010; Noble et al. 2012). Two recent fMRI
studies have reported SES differences in the function of certain language-supporting brain regions, namely the left fusiform (Noble et al. 2006) and left inferior
frontal gyrus (Raizada et al. 2008).
Epigenetic research plays a twofold function in this context. First, it provides a
key missing link to explain the molecular pathways by which transient environmental factors can leave marks or be inscribed on the biological body. The often
elusive role of social factors (poverty, inequality, stress, etc.) in affecting body,
brain, and behavior is likely to find a less ethereal mechanism in epigenetic
mutations (Champagne 2008; Miller 2010; Vineis, Stringhini, and Porta 2014).
New Genetics and Society 139
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Obviously, if the trend toward transgenerational epigenetic inheritance consolidates, the mechanism will involve the exposed as well as unexposed generations.
Second, epigenetics represents the conceptual climax of a more profound
appreciation of the many material flows connecting the wider environment and
the body (Niewöhner 2015). I will conclude this section looking at the potential
present in epigenetics to move toward a more ecosocial view of embodiment
(Krieger 2011), beyond superficial interactionism.
The epigenetic body: embodied constructivism beyond the genetic body
Several works have recently emphasized the potential in the epigenetic discourse of
undermining the still influential idea of a body autonomous and insulated from its
material surroundings. Especially when understood in a broader ecological sense,
epigenetics becomes a perfect epitome for the extreme porosity between the milieu
and the body (Niewöhner 2011; Guthman and Mansfield 2013; Landecker and
Panofsky 2013).
Meaney’s experiments on the transmission of inadequate mothering in rats are
illustrative of this dynamic for which social events become regulative of the organism physiology. Certain behavioral exposures (low licking/grooming) shape
changes in methylation patterns which modify genetic expression and neurochemical responses in the brain. This modifies the physiology of the pups that, once adult,
will reproduce the inducing behavior and consequently modify their environmental
niche, thus shaping the biological life of the forthcoming generations.
In epigenetics, therefore, the dictum that “bodies express ecology” (Piersma and
van Gils 2011) seems to find a stronger confirmation. We are well beyond, as
Niewöhner insightfully writes, Western views of the individual as separated from
the external world by their “impenetrable” skin. An “altogether different degree
of entanglement between body and context” is brought to light (Niewöhner
2011, 12).
What is important to emphasize here is that this openness of the epigenetic body
to the world is a significant rupture with the mainstream lesson of twentieth-century
biology, especially genetics (Meloni and Testa 2014). The “genetic body” was built
on a segregation of the somatic from the genotypic level (Griesemer 2002). First,
through the Weismannian separation of the soma from the germ line (imperviousness of the hereditary material). Second, this passivity of the somatic level was
powerfully reinforced by the so-called central dogma of molecular biology
which stated that no information can travel back from protein to DNA.
Relegated to the passive end of the genetic chain of information (Gudding 1996),
the agency, situatedness, and reality of the body were elided in twentieth-century
genetics (Keller 2001; Robert 2004). Not by chance, as social epidemiologists
and historians of medicine have noted (Krieger 2011; Rosenberg 2012), the mainstream biomedical approach, with its search for inward causes, ended up viewing
the body as a passive biophysical abstraction with no serious consideration of its
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140 M. Meloni
embedding in local surroundings, nor appreciation of it being marked by material
and local contexts (Lock 1993, 2001, 2013; Lock and Nguyen 2010).
Against this marginalization of the body in twentieth-century genetics and biomedicine, epigenetics, especially when theorized in sophisticated conceptual frameworks, can be seen as a decisive advance toward what can here be called
“embodied constructivism”, a position that tries to overcome the shortcomings of
both reductionistic biomedical theories of the body and disembodied social constructionist views.
Although used sometimes in phenomenological contexts, the term “embodied
constructivism” is here named after the “constructivist interactionism” of developmental systems theory (DST). In the spirit of DST, it is meant as an invitation to
think in terms of non-dichotomous, jointly determined, and reciprocally contingent
biosocial factors when explaining human development and social life (Gray 1992;
Oyama 2000; Griffiths and Gray 2005). Expanding on the “parity thesis” of DST
(i.e. equality between the role of DNA and non-DNA elements in explaining development), embodied constructivism defines a non-hierarchical and relational ontology in which social structures can be seen as the sources, as well as the effects, of
biological factors. There is a genetic component to social processes, as there is a
social shaping and driving of genetic expression (Landecker and Panofsky
2013). Biological realities always emerge socially situated and “interwoven with
meanings” and culture is always in human biology (Goodman 2013).
A good example of what I mean by embodied constructivism is the recent work
by Clarence Gravlee on the material pathways through which “race becomes
biology”. The article explores the double biosocial movement by which racism
and social inequalities (as a sociocultural categories) are embedded and materialized in the “the biology of racialized groups and individuals”; while at the same
time embodied inequalities (the biological level) perpetuate and reinforce “a racialized understanding of human biology” (Gravlee 2009, 54).
Epigenetics can fruitfully complement this line of thought: the body bears the
inscriptions of its socially and materially situated milieu, and the milieu is constituted by the socially modulated present and past biographies of the body (nutritional, metabolic, behavioral, toxicological, psychosocial, cultural, etc.).
Not only is genetic expression socially modulated (that is influenced by power
structures in society), but it is also the source of novel environments that will shape
in their turn the “socially modulated biologies of further generations of organisms.
The causal arrows go both ways, and the ontology of the gene as content and the
environment as context ceases to make sense” (Landecker and Panofsky 2013, 351).
Critical coda: soft-inheritance and its quandary
I have mainly focused in my article on the theoretical potential of epigenetics to
bring together biology and the social sciences after the acrimonious conflicts of
the twentieth century, conflicts partly determined by taking a narrow view of the
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New Genetics and Society 141
biological and equating heredity with transmission genetics. In the light of this, it
would be tempting to say that, in the novel postgenomic scenario, we finally have
the opportunity to speak of the biological in the social sciences with less anxiety
about biomedical reductionism or the return of eugenics. Although tempting, it
would be more careful to postpone this claim. The reason for this cautiousness
comes, in my view, from two main lines of argument.
First, there are too many uncertainties not only about the biological significance
of the epigenetics revolution but also about which stakeholders are going to prevail
in the epigenetic arena. It is far from obvious that gene-centrism will be effectively
overcome rather than reinforced by epigenetic findings (Lock 2005, 2012; Richardson, forthcoming; Waggoner and Uller 2015). The epigenetics revolution has been
compared to the Gramscian passive revolution (Meloni and Testa 2014): a revolution that is less a radical break and more a limping compromise with existing forces.
The analogy seems valid especially in the sense that underneath the surface of
hyped claims about a rupture with gene-centrism, the prevailing tendency is to
use epigenetic marks as a sort of “fifth letter” of the genetic code and a tonic for
the unkept promises of various genetic projects.
A second, different but likewise important line of critical reflection originates
from opposite reasons. It is the possibility that a new epigenetic approach will
prevail in wider society as a distinctive way to understand the relationship
between human beings and their biology. It is possible (much more so than three
decades ago) that hard-heredity will no longer be considered the only game in
town. This idea has been at the center of my article: with the advent of epigenetics,
a paradigm is emerging that is very different from previous articulations of genetics
and society. If we look at the two main implications of epigenetics for the social
sciences as I have described them: (1) the denaturalization of the genetic lottery
and (2) the deepening of the notion of embodiment – what seems to emerge as
common point is the erasure of any residual distance between the biological and
the social in the ontology of human beings.
To reiterate the previous findings: present social contexts get under the skin and
deeply impregnate our biology; various past environmental events shape our
genetic lottery, at least at the level of its expression; local social events become
embedded in human biology potentially contributing to differences and variation
amongst human groups. The bottom line is that a demarcation between the biological and the social becomes increasingly untenable.
However, this blurring of the line between the biological and the social may
assume several contradictory guises in society, with unpredictable effects upon
moral reasoning. What it is often too easily forgotten is that the separation of the
biological from the social established by hard-heredity played a complex conceptual and political role in the early twentieth century. In favoring an emancipation of
the sociocultural from its biological bases, hard-heredity became (somehow paradoxically) a helpful construct for cultural anthropologists eager to get rid of the
“vitiated mixture” (Kroeber 1915) between the heredity and civilization,
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142 M. Meloni
symbolized by the Lamarckian trends in social sciences (Stocking 1968). It is undeniable that Kroeber, one of the fathers of cultural anthropology, saw in hard-heredity his best ally to get rid of racialist discourses that were part and parcel of
neo-Lamarckian social science (Stocking 1968; Kronfeldner 2009). Of course,
there was an awful lot of racism also amongst Mendelians (as Boas well knew),
but Kroeber thought that by taking advantage of the separation of heredity from
culture, this latter (aka the Superorganic) could become a space that is much
more malleable by human effort.
If we are heading therefore toward a potentially neo-Lamarckian situation where
social experiences can become part of our biological memories, we need to consider carefully what this may imply for the social sciences. Leaving aside ontological questions about the robustness of the category of the “social” (and therefore of
“social sciences”) in a situation of continuous osmosis between “the biological”
and “the sociocultural”, some more directly political questions remain to be
answered for the epigenetic scenario.
For instance: How will the plethora of epigenetic studies showing how various
traumas travel across generations be translated into public policy? How complete
will the identification be between specific groups and the pathogenic environments
to which they have been historically exposed? Will this become the basis for reproducing and consolidating structural differences in society (class, gender, and race)?
What if epigenetic discourses on different levels of methylation between social
groups are used to underwrite new discourses on “the biological inferiority of
the poor” (Katz 2013) or on an incapacity of the poor to seriously take care of themselves (Mansfield 2012)? Will the embedding of the body in its own socioeconomic
context become so profound as to be seen as an unbreakable chain? Or will the
novel emphasis on the reversibility of epigenetic signatures always keep open
the possibility of change even for the most “damaged” social groups?
It is likely that the answer will be somewhere in between this two. As Eva
Jablonka has pointed out (personal communication), a critique à la Filipchenko
on the permanent scars left by historical oppression on the proletariat is based on
the idea that with time epigenetic effects become more difficult to reverse. This
does not need to be, however, as the reversibility of epigenetic signatures can
depend on different factors, such as the persistence of certain environmental conditions, etc. Epigeneticists seem in sum more optimistic today about the easy reversibility of epigenetic marks. Scientifically, this may be a satisfying answer, but the
political conditions in which the costs of reversing bad epigenetic signatures will
take place are not for scientists to decide. We too often take for granted the naturalness of our human rights framework in which we expect epigenetics to help promoting better schools for children, or more serious cures for traumatized people.
However, what the last century has taught us is that when the broader political
conditions deteriorate, even good scientific ideas such as Mendelian inheritance
can easily be turned into ammunitions for race or class discrimination. Therefore,
in principle, the relatively easy reversibility of epigenetic marks should be a
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New Genetics and Society 143
reassuring answer against fears of a new biological racism or classism under epigenetic guises. However, how costly for society this reversibility will be is not in the
hands of scientists. Cost –benefit considerations on the availability of public
resources to invest on such policies, or political considerations on the opportunity
to do so is not a scientific but a political decision.
These are the set of problems to which this article has no answer, but nonetheless
need to be raised to set the perimeter of the specific ethos of our postgenomic world.
Certainly many of these social sciences translations appear speculative at present,
given the uncertain status of epigenetic research and, particularly, transgenerational
inheritance, as said above.
However, we must also not forget that much of the science behind eugenics (the
unit of character hypothesis for instance) was, to say the least, precarious and controversial at the time (and in the end wrong), but this did not stop a direct translation
of these scientific arguments into harsh policy measures, under certain existing conditions of “law and sentiment”, as Galton would have said. My mixed conclusion is
that, as usual in the history of how biological arguments are imported into the
public sphere, there is no one-to-one relationship between scientific theories and
social values (Meloni, forthcoming): much will depend on the broader socio-political context in which science circulates.
Epigenetics has lots of potential to rethink the relationship between the biological and the social world. However, even the best conceptual framework may be
open to the most unpredictable and sometimes unfortunate socio-political
outcome. This is why social and political scientists need to be prepared to the
many nuances of the novel scenario.
Acknowledgments
Thanks to Eva Jablonka, Danielle Allen, Didier Fassin, and Alexandre Guerrero for helpful comments
and bibliographic suggestions on the text. Of course, all the responsibility for the claims made is
exclusively mine. Thanks as usual to Andrew Turner for his help with the English language in the
text. Thanks also to John Dupré and the Egenis Centre, College of Social Sciences & International
Studies, Exeter University (UK) for offering me an Honorary Senior Lectureship that has be very
helpful in carrying out this research.
Disclosure statement
No potential conflict of interest was reported by the author.
Funding
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”), of a CAS/University of
Nottingham pilot grant on epigenetics, and of a Institute for Advanced Study (School of Social
Science), Princeton, NJ, annual membership funding.
144
M. Meloni
Notes
1.
2.
3.
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4.
5.
6.
7.
8.
See a subsequent work by the same group on the transgenerational effects (on the male line) of
smoking during puberty in Pembrey et al. (2006).
Often, a technical distinction is introduced between inter-generational (or parental) and
transgenerational effects, with the former shorter and limited to two generations, and the
second spanning over multiple generations (see Grossniklaus et al., 2013; Heard and
Martienssen, 2014).
A recent interesting update on epigenetic inheritance is Dias and Ressler (2014) study on the
transgenerational effects of olfactory sensitivity in mice. See for a comment Szyf (2014).
It is the case of so-called luck egalitarians for which any inequality of fortune, that is
beyond one’s control, no matter whether natural or social, needs to be corrected in society
(for instance in authors like Cohen and Dworkin; see for a critique Anderson, 1999). A
similar disregard for the difference between natural and social in the cause of unfair situations
applies in principle also to a full-fledged consequentialist position, for which what matters is
the nature of the outcome.
Although the key “moral” distinction in luck egalitarianism, which is between option luck and
brute luck, that is between choices and circumstances (Anderson, 1999; Tan 2012) may also
be in trouble in an epigenetic view.
The core of Fukuyama’s argument was against the idea of the genetic supermarket, i.e. replacing
the blind genetic lottery with consumerist choices of engineered reproduction that would
eventually “increase the disparity between the top and bottom of the social hierarchy” (2002,
157).
See the title “Babies born into poverty are damaged forever before birth” in the newspaper The
Scotsman as a comment to an epigenetic study on social exposure in the city of Glasgow, UK
(McLaughlin 2012).
A study on the negative transgenerational effect of lack of folate in mice diet (The Economist
2013).
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