Life-in-the-making: Epigenesis, Biocultural environments and human becomings 1

Eugenia Ramirez-Goicoechea

3rd DRAFT.
Original in Ingold, T. & Pálsson, G. eds. 2013. Social Becomings. Integrating Social
and Biological Anthropology, Cambridge: CUP. 84-105
http://www.cambridge.org/aus/catalogue/catalogue.asp?isbn=9781107025639

“In my opinion the greatest error which I have committed, has been not
allowing sufficient weight to the direct action of the environment, i.e. food,
climate, &c., independently of natural selection. … When I wrote the
'Origin,' and for some years afterwards, I could find little good evidence of
the direct action of the environment; now there is a large body of
evidence, …”. Charles Darwin to Moritz Wagner, 18762

Abstract

In this paper I will explore how human material-symbolic practices affect our
biologies through developmental processes such as epigenesis. Sociocultural and
political practices of power, inequality, deprivation, discrimination and social exclusion
from economic and social welfare, nutrition, health and care, education, produce
complex environments for specific biologies to develop and grow with(in). Human
becomings as developmental and evolutionary processes of life-in-the making, depend
on a complex regulatory systemic network of biochemical, cell, histological, organic,
and bodily non-linear interactions within itself and with its extrasomatic
environments. Epigenesis is an on-going developmental process of when, where and
how genomic materials are expressed or silenced in the cell and its biochemical
network, which, in turn, may feed back onto further genomic activity.
Biopsychosociocultural individual experiences related to anthropogenic environments
of socio-political and economic exclusion, and life-styles of deprivation,
undernutrition, and stress, may trigger specific hormonal, metabolic and
neuropsychological responsiveness and corporal states. These may activate or silence
epigenetic processes associated with the risk of health sufferings and disease,

1
This paper has been possible by a sabbatical leave (2009-2010) from my university (UNED, Madrid,
Spain) that I enjoyed at the Human Systematics Laboratory of the Universitat de les Isles Balears (UIB,
Majorca), thanks to the academic generosity of Prof. Camilo Cela Conde. I appreciate very much Dr.
Nancy Konvalinka’s help in taking over some of my academic duties during that time; also for her kind
revisions concerning my written English. I am also grateful to Daniel Lende for useful comments on an
early draft of this paper presented at the EASA 2010 Conference, Maynooth University (Ireland). I
thank Tim Ingold and Gissli Pálsson for organising such a fruitful workshop. This paper is dedicated to
the Biosocial Becomings team that was born on that occasion. Its epistemological and theoretical
framework follows an interdisciplinary biopsicosociocultural approach. This implies the need for an
enough sounded literacy in quite a few disciplines. Although references and notes have been reduced to
a minimum, I apologise for possible overwhelming citations. I also wanted to provide a tentative map
of possible itineraries for those interested in exploring some issues in more depth.
2
In (Darwin, 1887), vol.3:158. In http://darwin-online.org.uk/secondary.html
1
impinging on people’s employability and social mobility, reinforcing, therefore, their
social exclusion.
Our materialsymbolic worlds are not only relevant for individual developmental
life courses. Either by the parental/ancestors male/female germ line (in the gamete) -
as environmental family legacies -, or through embryo-foetus-child biochemical
relations with the mother/carer during the pre, peri and/or postnatal period, including
rearing practices, specific epigenomic states may be passed/produced in offspring,
their progeny and further generations without affecting their DNA. Crossgenerational
cycles of illnesses and disease may bolster the defranchisement of people,
perpetuating their social exclusion into their descendants, reproducing social closure
and inequality over time.

Key words:
Epigenesis, Biocultural Anthropology, Developmental Systems, epigenetic inheritance,
stress, social exclusion, race

X.1. From Genomics to Epigenomics. Epistemic and theoretical shifts

X.1.1. Genetic determinism. Flaws and misconceptions

When Mendel’s experiments and theories were rediscovered by Hugo de Vries

(1848-1935), Darwinian evolutionary theory conflated with genetics in what
J.S.Huxley named the New synthesis and Romanes, neo-Darwinism, because of its
insistence on natural selection. Instead of concentrating on organisms and their
evolution, the new evolutionary theory was interested in genes as the structural units
of inheritance, selection and evolution. Genes were defined for the first time by W.
Johannsen in 1909 (Johannsen, 1909):124. cit. in (Gerstein et al., 2007). They
became the units of heredity (Noble, 2010) and evolution, as items that contained the
instructions for building phenotypes from genotypes.
Gene-centered evolutionary theories reduced Biology to Genetics and life
evaporated from Biology (Ingold, 1990). Neither the shift from individuals to
populations (Dobzhansky, 1951 (1937)), nor that of genes to DNA (Watson and Crick,
1953) changed this genetic fetichism of Neodarwinism but reinforced it.
Genetic determinism is the hegemonic theoretical perspective both in academia,
the research agenda (cf. International Human Genome Sequencing Consortium,
2001); (Venter et al., 2001)), including allocated public and private fundings. It has
entered deeply into the mass media, orientating science popularisation, public
knowledge and popular culture.

Notwithstanding, genetic determinism, as early criticised as ignored, has

progressively been scrutinised as problematic due to several interrelated flaws and
misconceptions:

Complexity and non-linearity in life processes and their change over time

Neodarwinian biological and evolutionary genetic determinism is unable to

account for biological complexity. Organisms cannot be reduced to DNA and changes
2
in its information. Biological complexity cannot be predetermined genetically (Rose et
al., 1976). No single gene has been empirically proved responsible for the variation of
a complex phenotype (Plomin and Ho, 1991) neither for any supposed predisposition
to inherited disease (i.e. autism spectrum disorders, Alzheimer, cf. (Lock and
Nguyen, 2010:339&ff.)3. All phenotypic traits and outcomes are highly polygenic
(Shao et al., 2008).
As complex non-linear systems, biological systems do not follow the
superposition principle: global changes cannot be explained by the sum of
modifications in parts (additivity); change is neither similarly spread throughout the
system (homogeneity). There is not a specific one-to-one gene for any trait but a
many-to-many relation between genomic materials and phenotypic emergences 4. The
effect of genes is indirect and manifold within multiple hierarchical (horizontal and
vertical) biochemical systemic relations within the cell. There is stochastic causality:
there is selection within a limited range of possibilities. Life and evolution are
ultimately indeterminate (Lewontin, 1978).

Bounded discreteness of the essentialised gene

Although a variety of meanings throughout the 20th and 21st centuries5, the most
prevalent concept of the gene has been that of a segment of a macromolecule called
DNA that resides in the nucleus of the eukaryotic cell and carries the necessary coded
information for protein production that in the end will produce a specific trait. That is,
the gene is a bounded discrete unit that is part of reality.

A computational digital approach to the genome

In Neodarwinism and Genetics the gene has been mainly conceived as a digital
code of instructions (information) of which its order, its grammar, could be deciphered
from its signs. But DNA does not encrypt anything because there is no message per
se whatsoever. DNA can only be read in the growth process of the organism. Void of
context, the genome is an abstraction, a product of modern scientific invention
(Ingold, 2004:214,215).

Nature: environmental realism

Evolutionary theories rely heavily on an adaptationist paradigm of evolution,
which for human behaviour is grounded on a rationalist theory of decision and action,
the neoclassical economy paradigm of self-interest and methodological individualism.
If they want to survive, organisms have to adapt to Nature, a pre-existent reality that
imposes itself onto all living and non-living things as an external environment, as the
world-out-there6. Nature challenges the individual (and or a population) by posing it
3
Contrary to current traditional thinking, there is not a gene for blue eyes but a genomic
developmental process that disables the production of brown pigment (Moss, 2001):87)
4
So-called genes do not code for this or that phenotype but for the impact of environment on the
organisms’ development (Gould, 1977). The level of selection is the organism, the phenotype (Keller,
1999).
5
As a discrete, bounded, self-replicating unit of heredity, a distinctive locus of DNA, an action
programme for proteins to follow, a physical molecule, a code to be transcribed, a genomic entity that
can be sequenced digitally, an annotated numbered genomic entity in gene data bases. Cf. Gerstein et
al., 2007. As subroutines of a gigantic operative system also (Keller, 2005).

6
Sometimes as a generic and spatial-temporal empty environment for different forms of life to inhabit
in, prior to any kind of already in-built niches for organisms to develop and evolve within (Griffiths,
2004).
3
problems and hardships to-be-solved within a limited range of resources. But there is
no way of saying a priori what a resource can be for an organism to do something
with it. Challenges and resources are defined locally depending on many interrelated
proximal and distal factors. Therefore, we can say that there is not a single common
environment for all kinds of organisms7, less for social ones, in their variegated
ethnographical and historical eco-relations ways of relation (Pálsson, 1996; Descola,
1996).

Development and ontogeny neglect

Gene-centered biology, evolutionism, ecology and cognitivism 8 have
systematically ignored development and ontogeny. Johannsenn’s (Johannsen,
1911(1910)) reinterpretation of Weismann’s germ plasma theory established as
dogma the non-reversibility of the genotype/phenotype barrier 9, eliminating any
possible evolutionary consequences – Lamarckian or not - of behaviour, action and
ontogeny (see bellow). It was the genotype (germinal plasma) that was the sole thing
that descendents would inherit from their ancestors: acquired qualities could not be
inherited. Development and phenotype were (and are) reduced to the combined
effects of the genetic program with external environmental factors, the G+E equation.

The Nature/Social-Culture divide

In line with Western dualistic epistemological tradition, neo-Darwinian
evolutionists, biologists and cognitivists, have maintained a strong Nature/Culture
divide, giving pre-eminence to the first in the form of Physics and so-called “Life
Sciences”. Human behaviour and culture - the “extended phenotype” (Dawkins, 1976,
1982) – is naturalised applying to them the genetic determinism and natural selection
paradigms.

X.1.2. The Post-genomic turn.

In the 80’s a more systemic and dynamic perspective on Biology claimed for a
less reductionist view of the genome. The human gene enumeration and description
(International Human Genome Sequencing Consortium, 2000; Venter et al. 2001),
could not offer a complex enough account of how biological processes started up and

7
Even organisms, dead or alive, can be environments for other organisms, i.e. whale carcasses that
may feed marine worms for more than 20 years (Wiklund et. al.: 2009).
8
Including those fields that take this for granted: i.e., Behavioral Ecology ((Standen and Foley, 1989)),
Sociobiology ((Hamilton, 1964); (Trivers, 1971); (Wilson, 1975)), Memetics (Dawkins, 1982);
Evolutionary Psychology (Cosmides and Tooby, 1994); (Pinker, 2002); (Buss, 1994)) and Neodarwinian
Cognitivism.
9
Cases of inter-organismic gene assimilation are adding controversy to this dogma.
4
worked in an interlinked fashion (Keller, 2005)10. In 2003 the ENCODE (Encyclopedia of DNA
Elements) Consortium was founded, encompassing now more than 81 research institutions. It has provided
On the one hand, the bounded concept of the gene started to be challenged. We
cannot properly tell where a gene starts or ends. DNA segments splice, shuffle and
reshuffle, swap and shift places, as a condition for protein production (Pearson,
2006). They recombine and interact dynamically with other genomic, cell, histological,
hormonal, physiological and anatomical network systems. Nearly 43% of the
sequences that compose our genome are transposed from one place to other.
Dynamic processes of transposable and retro-transposable elements, copy number
variations, etc. suggest that genomic DNA variability is much higher than previously
thought (Charney, 2011): secs.4.1 & 6).
Nearly 98.5% of DNA does not code for any proteins. Composed mainly of
repetitive sequences and because of its unkown function, it was previously called as
junk DNA. However, 80 % of DNA has important biochemical functions particularly
outside the protein-coding regions (ENCODE, 2012). These non-protein-coding
transcripts have, however, an important role in a complex transcriptional organization
of interleaved protein-coding an non-protein-coding transcripts that questions the
currently physical boundedness conception of the gene; transcripts are important for an operational
definition of the genome (Gingeras, 2007).
This DNA plays a decisive role as a regulatory reservoir, contributing also to
other fundamental architectonic molecular structuring such as repairing damaged
DNA, sometimes becoming even the main acting component beyond the coding
sequence itself (Shapiro and Sternberg, 2005). The standard view of the RNA
molecule as only a transcriptional factor has also been empirically questioned: not
only it may produce proteins during development thanks to modified small mRNA
transcripts, but RNA has an important role interfering in gene expression (RNAi).
Hence, genomic materials cannot be specified independently of their dynamicity
within a whole hierarchically organised network of regulatory systems that interact
with each other at specific times and places within the cell (El-Hani, 2007; Pardini and
Guimaraes, 1992). The emphasis is on what type of biological function these
sequences intervene in and when and how they do it.
We could think then of a reactive genome activated, stimulated and partly
regulated by the dynamic interactions of cell activity and its environmental signals
(Shapiro, 2005:93). Cells regulate genetic engineering of genome system
architecture by specifying and demarcating its products, their specific linking and
10
The ENCODE (Encyclopedia of DNA Elements) Project has provided a huge corpus of research and
knowledge for such an endeavour. The project “provides information on the human genome far beyond
that contained within the DNA sequence — it describes the functional genomic elements that
orchestrate the development and function of a human. The project contains data about the degree of
DNA methylation and chemical modifications to histones that can influence the rate of transcription of
DNA into RNA molecules… also examines long-range chromatin interactions, such as looping, that alter
the relative proximities of different chromosomal regions in three dimensions and also affect
transcription. Furthermore, the project describes the binding activity of transcription-factor proteins
and the architecture (location and sequence) of gene-regulatory DNA elements, which include the
promoter region upstream of the point at which transcription of an RNA molecule begins, and more
distant (long-range) regulatory elements. … … ENCODE catalogues the sequences and quantities of
RNA transcripts, from both non-coding and protein-coding regions” (ENCODE et al., 2004). See also
(ENCODE et al., 2007)

5
cooperativity allow for the integration of responses and reactions. As the
immunological system shows, the cell’s natural genetic engineering contributes to
enhance efficiency searching for the genome configurations that encode functional
complex systems and favours the hierarchy of system architectures, even taking
control in DNA restructuration (Shapiro and Sternberg, 2005):96-97). At the cell
level, physiology cannot be separated from genomic regulation (Shapiro, 1999; Stotz
and Griffiths, 2008).
The time have come for a new conceptual description of the gene. As these
biological processes and their outcomes are stochastic, probable but within
constraints (Theise and Harris, 2006), so that we cannot predict for sure the role of
genes without the complex regulatory dynamics they are enmeshed in, combinatory,
diffuse and soft logic models, and semiotic and linguistic metaphors seem to describe
its complexity better. Self-organisation, mutual historical constitution of parts and
whole, global dynamics and emergencies in the cell, interconnection and
intercommunication of signals and networks, upward hierarchy and the relative
coherence of biological processes between contingency and determinacy, and a new
lexicon that favours interdisciplinary understanding, have been put forward for a gene
concept beyond itself (Keller, 2005).
Gerstein and cols. (2007:676) suggest an operative definition that should
include the following conditions: that is compatible in retrospect with the phenotypic
field with which it has been traditionally linked; that can be applied to any organism;
also simple and understandable, specific and practical for analysis and description;
and last but not least, that is consistent with phenomena and processes and their
nomenclatures. Thus, “the gene is a union of genomic sequences encoding a
coherent set of potentially overlapping functional products” (ibid:678)11.
The major bifurcation that this non-linear and complex systemic shift in Biology
has produced in the biomedical research agenda cannot be ignored 12.

X.2. Ontogeny and Development. Towards epigenesis.

X.2.1. Organisms as developmental systems.

Developmental Systems Theories (DST) (Oyama, 1985; Oyama, 1992; Oyama

et al., 2001) have contributed decisively to re-thinking life processes and their
dynamics in terms of development. So has a relatively new interdisciplinary field
known as Developmental Sciences for the social and political aspects of the life course
(Magnusson and Cairns, 1996).

Ontogeny is the process of development that takes place through the

organism’s life-course (Robertson, 1996). Organisms’ capacities and activity are the
11
Lenny Moss (2001:88) has suggested a Gene-D(evelopment), as a developmental resource, a
transcriptional unit that contained molecular template resources – i.e. specific nucleic acid sequences -
that might produce different genetic products that are biologically active or not at different
organisational levels and developmental stages. Operating at low levels of biological organisation and
with no “phenotypic outcome preinscribed,” the possible causal role of a gene-D is only conceivable
post-facto, within a specific interactional context and perspective (ibid.:89).

12
From structural genomics to functional genomics, from genomics to proteomics, from monogenic
disorders to multi-factorial disorders and the monitoring of susceptibility, from gene action to gene
regulation and the analysis of multiple genes in gene families, pathways and systems, from mutations
to pathogenesis (Peltonen and Mckusick, 2001). See further.
6
outcome of the emergent properties of developmental systems. Developmental
processes are generative and relational fields for interactions and forms to emerge
(Ingold, 1991; Lewontin, 1983). They are the product and locus of previous embodied
histories of regular interactions and experiences -as effective-enough statistical
patterns – that have sculpted the organism life and, in doing so, opened up further
paths of stability/change (Lehrman, 1953).

X.2.2. Ontogeny and Evolution

A shift in considering organisms’ properties as developmental processes – at

multiple complex and hierarchical levels – is becoming unavoidable, both in
Postgenomics, Evolutionary Developmental Biology (Evo-Devo), Evolutionary
Epistemology(EE) and in evolutionary thinking in general (Müller and Newman,
2005:487).
If phylogeny is about continuity/change in respect to other species, ontogeny is
about continuity/change within the organism’s own species and discontinuity with
others.
It is in the organism where ontogeny and phylogeny are specified by each other
(Gould, 1977). Ontogeny creates life and evolution, because all changes take place in
developmental processes (W.Garstang, 1922, cit. in Hall, 2000). Genetic activity is
not independent nor is it outside of the organism’s developmental system (Gottlieb,
2001:47,48). Development is not a factor of biology or of evolution but the very same
condition for both; it creates certain possibilities for evolution to act upon 13. The
organism as a developmental system becomes once again the scenario of life and
evolutionary change, as a multiplex dynamic field of/for action (Bateson, 2005; Mayr,
1999 (1942)).

X.2.3. Epigenesis

Epigenesis is the crucial concept from which the argument of this paper stems,
regarding the biosociocultural and political constructions of our local developmental
biosocialities.
If epigenesis originally referred to the modulation of non-DNA-based genetic
activity, now its meaning covers wider and more complex processes. Epigenesis is
the directional molecular process of genetic activation, expression, revelation,
suppression and regulation (Ho and Saunders, 1979; Monod, 1970). It is the
developmental process of what, how, where and when genomic materials are
silenced14 or expressed, through guidance and regulation of genomic products – i.e.
regulatory genes – in a vast system of developmental regulation.
Mainly by methylation and histone acetylation –but not only - DNA exposure and
access for transcription, protein and enzymatic activity and transformation is either
opened up or closed. Integrated regulatory mechanisms of proper environmental

13
As an interesting example a development-producing structure that, in its turn, constrains further
development, dental disposition in mice shows that the first molar is bigger than the following one. In
turn, the second is bigger than the third one coming after it. Molar development follows an inhibitory
model in succession. Dental development establishes, indirectly, the course for other changes to impact
the organisms in a specific way, i.e., the effects of a change in diet due to ecological transformations
(Kavanagh et al., 2007).
14
Most biomedical research concentrates in those genes that have not been expressed (in due time and
place) and not on those that have been and may cause a disorder.
7
signals and their combination with specific activational factors determine which
sequence will be recruited for transcription, when and where, including its beginning
and ending, what coding and non-coding parts will be spliced, how the remaining
parts will be reassembled and, if so, translated, what nucleotides will be inserted,
substituted or deleted, and what novel nucleotide information will be produced in the
sequence of genomic products (Stotz, 2006). The ensemble of transcriptional factors
and their binding events that specify the on-and-off states of genes in a
combinatorial fashion constitute cell’s regulatorycomplex network (ENCODE,
2012:91).
Epigenesis intervenes in the cellular division of the egg, the specialisation of
pluripotent cells for physiological processes, tissue construction and growth, and other
biological operations of further hierarchical complexity. From a single cell (zygote),
patterns of silencing and amplification of genome products produce the nearly 200
different stem cells that generate specialisation and functionality through cell
diversification. Cellular differentiation is governed by what C. Waddington (1957)
coined as epigenetic landscape a very complex panorama of networks and feed-
forward loops that make stem cells go into a lineage or not .
As a developmental process, epigenesis is highly context specific, following a
chronological and topological logic. Especially during the embryonic phase for normal
development and further specificity of tissues and organ functions, certain genomic
material must be in the right place at the right time for the cell to assemble in a
three-dimensional way with same neighbouring cells. All through the life-course,
epigenetic processes remain environmentally sensitive to the complex biochemical
processes in the cell and its interactions with other cells, at the tissue and organ level,
and the impact of the endocrine system onto other physiological systems.
Variation in expression/silencing and regulation does not entail DNA sequence
changes, either nuclear or mitochondrial. Phenotypic differences in local biologies are
mainly due to the functional absence of a resource present at a specific time and
place in an interactive network of biochemical interactions. Compared with the
genome, the epigenome – as the epigenetic state of a cell at a particular moment - is
very dynamic and is in constant flux.
On and off genomic expressions may occur very early during the embryonic
stage, being “generatively entrenched” (Wimsatt and Schank, 1986), directing and
orientating further developmental and epigenetic paths. This has been called
epigenetic (re)programming.

Changes that promote DNA accessibility or closure for transcript factors to act
upon, are like tags, called epigenetic marks. Present in either parent’s gamete –the
sexual cell – or in both, they may be incorporated in the zygote, and maintained
during mitosis and further cellular divisions of the egg and cell specialisation. This has
been called epigenetic inheritance of which its molecular and biological mechanisms
and organisation seem to be very complex (Goldberg et al., 2007) (see further).

Epigenetic marks can also be produced ex-novo at any period of time,

depending on biochemical events related to embryo, foetal, child, adolescent or adult
experiences15. Many diseases can be explained by complex epigenetic processes in
different moments and periods of the life course. More than 90% of breast cancers
15
So can germ-line inherited epigenetic marks for disease propensity be reversed: the saying can go
like “if any of your parents was hypertensive, run at least half an hour a day”. Cf. (Shook et al., 2012).
See also below.
8
“are not associated with any germline mutation” (Moss, 2001:89) but to epigenetic
changes. Most cancers of any type are related to the aberrant methylation of gene
promoter regions (Esteller et al., 2001; Lin and Maher, 2010). Metabolic and
cardiovascular problems (CVS), inflammatory bowel, auto-immune diseases,
schizophrenia, and autism spectre disorders (ASD), among others, are also strongly
related with genetic silencing or expression during the patient’s life history.

As we shall go in more depth in next sections, epigenetic processes are also

sensitive to personal embodied experiences which produce/are produced by somatic
biochemical responsiveness to a diversity of environments. The case of monozygotic
twins is paradigmatic. Their case has been frequently selected as proof of genetic
determinism and its narrative. Very similar genetically - although not necessarily
identical (see Charney, 2011)- when born, they start to develop phenotypic
differences from each other even in similar rearing environments; as they grow older
these disparities increase. This happens mainly because of differences in DNA
methylation and histone acetylation, as biochemical differential responsiveness to
experience and life styles concerning diet and nutrition, exercise, restorative
practices, emotional experiences, life hardships, stress, etc., which also depend in
part on income, social status, etc. (Fraga and Al., 2005) (cf. infra.)

It seems about time to take epigenesis and epigenetics seriously (Pembrey,

2002; Jablonka and Lamb, 2002; Ho and Burggren, 2010).

X.2.4. Epigenesis, Phenotypic plasticity and Evolution

In development and phenotypic plasticity, what matters is the patterns of gene

expression (Keller, 2005:4). It is true that that evolutionary change and differences
between species are partly determined by changes in protein-coding sequences but
also by modifications that alter gene regulation. The phenotypic plasticity that
epigenetic changes can bring about explains part of the wide range of biodiversity we
encounter without having to refer necessarily to genetic mutations. Also in human
populations. African so-called Pygmies are much shorter than other people. There is
evidence that height have the same endocrine etiology in humans. Because a
defective response to the growth hormone (GH) during puberty, due to very low
values of baseline serum GH-binding protein (GHBP) and surge of the insulin-like
growth factor-I (IGF-I) these populations do not experience the growth spurt common
in human ontogeny during this period. It seems that both the Growth Hormone (GH)
and the Growth Hormone Receptor (GHR) are under-expressed due to complex
epigenetic regulations (Bozzola et al., 2009).

Epigenetic processes introduce another domain of variance for natural selection

to act upon. In times of stress, error-prone DNA replication and activation produce a
wide range of somatic variability. Epigenesis seem to tune this individual variability to
that of the environment and its pressures (Rando and Verstrepen, 2007)
Epigenesis is not a random process as natural selection is assumed to be, but a
stochastic phenomenon, probable but never certain (Waddington, 1942). When
environmental conditions change, cell physiology may change very quickly as well.
When changes are long-term, adaptability concerns the DNA. But when changes are
9
produced in an intermediate evolutionary chronology, the lapse between two and one
hundred generations, cell memory and epigenetic inheritance contribute to a good-
enough eco-relation with environmental changes (Jablonka and Lamb, 2005).
The evolutionary consequences of this flexibility cannot be underestimated.
Through novelty, innovation and origination (Müller and Newman, 2005:490 & ff)
phenotypic plasticity due to epigenetic changes may be selected in a population by
natural selection (Pigliucci et al., 2006; West-Eberhard, 2003)16. Midterm
evolutionary adaptability could therefore be understood as phenotypic flexibility
epigenetically inherited and environmentally directed, without having to wait for
natural selection of randomly produced mutations, which have a longer evolutionary
span.

X.3. Worlds of our (other’s) material-symbolic and political practices.

One of the main claims of this paper is taht our anthropogenic built
environments may induce certain epigenomic states and changes in our local biologies
but also at the population level, through the recurrence, institutionalisation,
modification, of our materialsymbolic practices. If genomic expression/silencing
depend on epigenetic processes and if epigenesis is environmentally sensitive, this
means that our anthropogenic environments and the experiences they may
individually or collectively induce have to be seriously taken into account in our
biosocial becomings during our life stories. This phenomena have been called
environmental inheritance17.

X.3.1. Niche construction and human agency.

Gene-centered Biology and its related disciplines do not consider the organism
(or any other unit) as a co-building agent of its surrounding but as a passive recipient
of evolutionary forces and environmental pressures dealt out by the natural selection
of random mutations. No evolutionary changes are to be expected from organism
activity (Simpson, 1953).
However, life-systems, even in their simplest form, are distinctive because of
their constructive eco-organisation of a relevant scenario, a generative field of forms
and relations, a landscape of variables for their own good-enough sustainability and
that of their progeny (Maturana and Varela, 1992). The concept of niche construction
accounts for this complex autopoietic process of action in evolution (Bateson, 1988).
Proposed first by Richard Lewontin (1982) and developed later by Odling-Smee
(1988) and others (Odling-Smee, et al., 2003; Day et al. 2003)), it claims for a
mutual constitution and engagement of organism and environment, including its
negative and positive feedbacks and possible co-ontogenies 18. Possibilities and
16
There is evidence of the evolutionary role of DNA methylation (especially cytosine methylation) in
animal genomes. It has been claimed that as much as 25% of the mutations that separate chimps
from humans occur at CpG sites, of which humans have only 1/5 of the expected proportion (Elango
and Yi, 2008).
17
Strictly speaking, environments are not inherited; rather, it is the material-symbolic world in which
we become the type of living creatures we are, hominised and humanised organisms, persons, to
develop and grow as part of a new generation.

18
Organisms, dead or alive, can be environments for other organisms, i.e. a whale carcass. As
primates with an omnivorous diet, our guts host millions of helpful bacteria with which we have
10
constraints (not rules) for organism development, growth, adaptability and
evolvability, depend on the history of its structural coupling with other living and non-
living systems with which it co-develops and co-evolves (Lythgoe, 1979). In that, as
particular forms of existing and being alive, organisms are both the object and the
subject of evolution (Lewontin, 1983) and development.

Organisms are particular places for growing and developing in the specific ways
of a relational world in which they unfold by means of their own life activities and are
unfolded in their own specific morphology, moving capacity, responsiveness and
epistemic and emotional awareness that the organism “grows into” (Ingold,
2004:216). As ecosystem engineers via niche construction, organisms are active
builders of their (and others’) environments, and, in doing so, they are agents of
change for themselves and for others19. Through continuous determinate/contingent
processes of action-in-relationality/relation-in-activity, objectivisation and
institutionalisation, along and through the generations, historically and culturally
situated humans build material-symbolic somatic and extra-somatic structures that
can be stabilised as scaffolding foundations (Shore, 1996), for other evolutionary
socioecological structurings to emerge in local time and space (Fuentes, 2009)
(Richerson, 2012).
For any human active eco-organisation, niche complexity is manifold, because
human(s) actions and practices are necessarily materialsymbolic. This means that,
for us, there are no material actions void of the symbolic/ideographic/discoursive
quality by which they are made possible by and for an epistemic community of
practices. By the same token, the symbolic, ritual, imageries, discourses and the like,
are not empty vessels to be filled in by a diversity of cultures, only acquiring their
existence as long as they are practically produced in a particular relational world. For
us, there is no ontological division between the material (Nature?) and the symbolic
(Culture?).

X.3.2. Developmental niches; home caring environments

The anthropogenesis of our sociosymbolic-material conditions of existence was

already mentioned by Karl Marx in A Contribution to the Critique of Political Economy
(1859), and in The Eighteenth Brumario of Louis Napoleon (1852), regarding how the
specific doings and makings of our forefathers (& mothers) reach the next generation,
providing them with the context in which they will develop and live their own lives.
We grow in environments built by the activity of our ancestors, which have
shaped our developing scenarios for making a life of our own (Ingold, 2004:217); we
will do the same for our offspring and their successors. Therefore, we can speak of an
ecological niche which is the possibility for our own human(ised) existence as active
recipients of our predecessors’ practices, representations and experiences, a world

coevolved (Ley et al., 2008). In that we may call ourselves metagenomic organisms.

19
The increased self-reproductive complexity of humans symbiotic sociomaterial inter-relations with
themselves, other species, artefacts, landscapes, and other non-living objects, has had an impact on
other organisms niches, environmental resources and climate change without any precedence on Earth.
Neolithic political, economic, demographic and social transformations were the definitive critical
bifurcation for what looks to be a never ending human eco-appropriation of all kinds of niches at the
cost of other organisms’ ways of life.

11
that we will inevitably change, as our children and grandchildren will also do when
carrying on their own existence.
Karola Stotz (2008) speaks of developmental niche construction as a set of
stable environmental non-linear interrelated resources that are provided by the
organism species’ antecessors, its “parents” and its own experience throughout life,
allowing it to develop in a reliable, predictable pattern of existence. West and King
(2008:384) call it “exogenic inheritance,” a reliable, probable and stable environment
over generations that, nonetheless, “can adapt rapidly to changing ecological
circumstances”.
This concept of an ontogenetic niche refers to how species-typical behaviours
develop through active, context-dependent processes within a complex
genomic/epigenomic regulatory system that includes molecular, cellular, ecological
and social (and political) experience, plus other developmental resources such as
social, cognitive and emotional stimulation in the pragmatical caring world of parents,
siblings, and others that provide 'nurturing' and affordances for development (Alberts,
2008a). The recurrence of the same or similar stabilised environmental
possibilities/constraints in the form of regular normally occurring sensory stimulation
influences genetic/epigenetic activity. Species specific similar environmental
landscapes induce probabilistic (Gottlieb, 1971) similar developmental systems in
organisms20.

Parenting/caregiving materialsymbolic practices of bonding and care as family

environments are critical resources for the provision of nutrition, protection and
sociocultural knowledge for children’s active balanced biopsychosocial growth and
maturity. As psychobiology and the anthropology of child-rearing and socialisation
have shown, parental (care-taker) care is one of the most powerful forces for
stabilizing the parameters of the ontogenetic niche. Nurturing activities, control of
alertness and sleep, attention, posture and body contact and manipulation,
perceptosensorial stimulation, selection of social exposure and its contexts, attention
guidance, formatting of communicative skills and direct and indirect speech, social
referencing, etc., are co-produced material-symbolic practices in communicative
sociocultural settings, in which the baby is an active part – either as direct or
vicarious participant, or as the subject-object of other’s practices - of this dialogical
relationship (Ramirez Goicoechea, 2009) 21.
Care, parenting styles, stimulation and home environment have a huge impact
as mediators of children’s early mental development, even in spite of low economic
status (Kim-Cohen et al., 2004). The impact of the quality of the home environment
on the child’s behaviour is higher when associated with socio-economic status (SES)
and the differential access to experiences and resources it provides, showing that it is
the complex combined effects of all variables that may explain differences in
children’s development (Bradley and Corwyn, 2002; Propper and Rigg, 2007). As
adoption studies show, genetic predispositions for some psychiatric disorders (i.e.
schizophrenia, autism spectrum disorder, attention deficit hyperactivity disorder, etc.)

20
I.e., the capacity for copulation in male rats is not innate but acquired in the most probable
environment that the developing rat system encounters (Ariew, 2006). See also Avital and Jablonka,
(2000).

21
If parents and caregivers make children, so do these to the first, in a non-isomorphic reciprocal
process. Among many other evidences, it has been reported that father-bonding with child lowers
testosterone levels on the male parent.
12
need the triggering force of the environment for its expression: genetic factors are
evoked in the child’s phenotype depending on the quality of the family caring
environment (Maccoby, 2000) and his/her active responsiveness.
A relationship between socioeconomic conditions and gluco-corticoid stress
response in childhood has been established in an ethnographic study in the Dominican
Republic (Flinn and England, 1997). It was discovered that this influence was indirect,
affecting children through the quality and intensity of child care. Release of cortisol
may help modulate perceived psychosocial and cognitive-emotional affronts, at the
cost of immunity and other health shields. Difficult family environments such as those
involving partner disruptions, caregivers with economic and emotional problems,
traumatic events, etc., affect the quality of care, with specific consequences for
progeny developing health problems, which also is connected with individual factors
such as the child’s vulnerability and resilience, depending on age, sex and personality
(Elder, 1974).
Childhood sexual abuse sets off disturbances in many interconnected systems
and subsystems of the body, potentially leading to a plethora of physical and mental
symptoms and disorders. It may concur with a multifactorial context of family
violence, separation or divorce, substance abuse, mental illness, or crime, the
intersection of which may produce a cascade of interwoven emergent effects
(Fullilove, 2009; Maccoby, 2000). In a study of adults with psychiatric illness, the
authors concluded that the impact of childhood sexual abuse on the illness burden was
"roughly comparable to the effects of adding 8 years of age". Its impact on daily
activities and body pain was even higher, as if adding 20 years of age to the
individual (Talbot et al., 2009).

X.4. Crossgenerational epigenetic effects.

X.4.1. Maternal and paternal effects. Intrauterine, peri- and postnatal environments

There is a growing body of evidence in animal models and human longitudinal

surveys and long-term family studies, showing that environmental influences have
complex ways of affecting the epigenetics of human biology throughout the life
course, especially during specific developmental stages. It is not that our socially built
environments directly trigger gene expression or silencing but, instead, they
constitute biosocial settings for particular developmental and growth processes
through biochemical and hormonal interactions. Somatic and extrasomatic
environments may induce epigenetic changes through biochemical organic
responsiveness to them and it is through these chemical and hormonal changes that
epigenesis takes place at the molecular, cell, tissue and organ levels.
What has been called mother epigenetic effects during periconceptional, fetal
and early infancy periods have a strong influence on the child phenotype and health.
The uterine and perinatal experiences of foetus and baby are developmental
settings22 in which the mother’s biochemical and hormonal situations may induce
specific dynamic epigenomic states in progeny (Gluckman et al., 2008). These
maternal effects of epigenetic transmission in mammals may have a huge impact on
22
“It is an inconvenient truth that the onset of behavior is before birth” (Alberts, 2008b:270). In
prenatal developing systems of experience (Gottlieb, 1997), “Each sensory system begins to function
while still undergoing maturation .. so each system could contribute to its own normal prenatal (as well
as postnatal) development” (Gottlieb, 2001:44-5). Only through function does structure realize in
development as a unified transactional event throughout time (ibid.).
13
the baby’s development and child and adult health during their life course. We remind
that some of these early embryonic and foetal induced states may become deep and
strong factors embedded in early ontogeny, working as stabilised structural
enhancers/constraints for further developmental processes.
Mother/foetus-baby biochemical, hormonal and sensory-motor
psychosocioemotional interactions in mammals take place especially through placenta
and umbilical cord exchanges, breastfeeding, and early stimulation, control and
regulatory behaviour23.
Through intrauterine influences on development, offspring of overweight and
diabetic mothers have a strong possibility of suffering from insulin resistance during
childhood and adulthood (Yajnik, 2004)24. The developmental foetal origins of some
cardiovascular diseases in humans has also been explained by epigenetic mechanisms
in foetus development under the label of the Barker effect theory (Barker, 1995;
2004).

While providing close body contact and the stimulating effect of the mother's
odour and heat for biospsychological emotional balance, breastfeeding bolsters
children’s immunity. Early development of gut flora by breastfeeding protects the
baby from further allergies, diarrhoea and inflammatory disorders and the risk of
diabetes type 1. Indulgent lactating mothers reduce offspring reactivity and anxiety
as responses to stress, being that the effects can be found also in the third
generation.

Increase of non-medically justified caesarean births prevents babies’ contact

with mothers’ vaginal flora, which is important for their own immune system building.
C-section increase the risk of type 1 diabetes by 20% (Cardwell et al., 2008); the
same percentage applies for asthma risk (Thavagnanam et al., 2008). Physiological
and psychological consequences of Assisted Reproduction Technology (ART) and in
vitro fertilization are also under scrutiny for its possible epigenetic consequences 25.

Although less known, paternal effects are also relevant. Father’s presence
and/or involvement in caring practices have been reported as having a strong
influence on off-spring accelerated maturation development in some multimale
primate societies (Charpentier et al., 2008). Analysing data from the ALSPAC Study26,

23
Studies of the Norway rat (Rattus norvergicus) evidence that suckling is not innate but the result of
olfactory stimuli of the mother’s body and hair that act as precursors of this behaviour while she
shapes the little rat’s behaviour into an exploratory search which ends up in finding the teat and then
suckling (Alberts, 2008a). The result of sexual differences in gene expression in the developing spinal
cord of rats is due to the difference in the mother’s liking of pups genitalia, which, in turn, is elicited by
greater expression of chemicals in male pups than in female ones (Moore, 1992).
24
Mice with a genetic propensity to develop cardiovascular diseases could have this propensity reversed
by changing their mothers’ diet when breastfeeding (Mcleod et al., 2007) and, therefore, gene
expression. See Conclusions for epigenetic reversals in humans.
25
Although low, manipulation of sperm and ovocytes in ARTs, especially if there are multiple births, is
associated with an increase in the risk of several birth defects such as cleft lip, cleft palate,
gastrointestinal and other problems (Reefhuis et al., 2009). It has been proposed that another risk
consequence of IVR may be epigenetic changes due to the methionine content of proprietary
commercial media used in ART that may be linked to children with Beckwith-Wiedemann syndrome,
Angelman syndrome, and retinoblastoma. Cf. (Niemitz and Feinberg, 2004). ARTs may also be linked
to some cases of attention deficit hyperactive disorder (ADHD). Ana Vidal, personal communication.
2004.
14
it has reported that fathers who had started smoking before age 11 had sons who had
higher body mass indexes; this did not happen with daughters (Pembrey et al. 2006).

X.4.2. Our ancestors’ legacies

Our ancestors legacies are a complex but intertwined process of interrelated

aspects: an environmental/ontogenetic niche, and a genomic/epigenomic legacy.
Practices, representations and beliefs concerning the social and political
distribution of health, diet and nutrition, gender and sexuality, hierarchy and decision
autonomy, work conditions, stress, trauma, exposure to pollution and toxics, etc., not
only have consequences for phenotypic plasticity at the somatic level. Our forefathers
and foremothers do not provide us only with specific anthropogenic extra-somatic
environments for playing out our lives. Parents and ancestors epigenomes, as the
global epigenetic state of an organism, may be incorporated in their offspring’s
gametes and then retained in the cell egg, in meiosis and in the cell’s further
divisions.
Incorporated in the germ line – although not in the DNA -, these epigenetic
marks may have important health consequences for the new generation in what
respects to glucose metabolism and diabetes, fat deposition and propensity to
obesity, regulation of blood pressure and other cardiovascular conditions,
neurophysiological response to stress, delay in neurocognitive development in infants
and children, food sensitivity, allergies, inflammatory bowel, cancer, etc. The
molecular mechanisms of this crossgenerational phenomena are still under
investigation. Let us provide some interesting empirical data that implies the study of
three generations.
Bygren, Kaati and Edvinson (Bygren et al., 2001) studied harvest and food
prices, demography and the health evolution of a small and isolated northern Swedish
town called Överkalix. They were able to establish a strong association between
ancestral food supply and longevity of third generations. They also showed a link
between food availability to ancestors and the cardiovascular and diabetic risk of
descendants (Kaati et al., 2002). They discovered that the correlation between food
access and reduction of longevity and the increase in cardiovascular and metabolic
risk only happened when it was their paternal grandfather’s who had access to food
supply during the slow growth period, established for boys in between 9 and 12 years
of age (Bogin, 1999 (1988)), before the pre-pubertal peak, when apparently less
nutrition is needed. Quite the opposite, the grandchildren of grandparents who
experienced famine during the same period were less prone to suffer from
cardiovascular conditions than those of ancestors who did better during those years.
Reanalysing the Överkalix data, Marcus Pembrey and cols. (Pembrey et al.,
2006) that those grandsons of grandfathers that experienced discovered that paternal
grandmother’s food availability was also associated with grandaughters mortality risk,
but not with that of grandsons. Some of Marcus Pembrey and colleagues conclusions
were: 1) a sex-specific male-line transmission linked to chromosome Y in humans, 2)
the relevance of the slow growth period in epigenetic marking, especially in

26
ALSPAC (The Avon Longitudinal Study of Parents and Children, formerly the Avon Longitudinal Study
of Pregnancy and Childhood) is a research project designed to understand the effect of environmental
pressures on the individual’s genotype and how the combine to influence health and development.
Until 201 data from nearly 10 000 children and their parents had been collected, from early pregnancy
until children were 8/9 years old. See http://www.bristol.ac.uk/alspac/
15
gametogenesis, which in males occurs during this period, and in girls mainly during
fetal life. 3. the short term response of the biological system to fast-changing
environments; and 4) the transgenerational effects of ancestors’ specific
environmental exposure and biocultural responses.
These epigenetic changes that appeared also in third generations did not affect
their DNA, nuclear or mitochondrial. Nor did these have to undergo the same or
similar experience their grandparents had to exhibit this epigenomic coincidence.
Another interesting case is the impact of famine on pregnant women and their
future babies during war periods. Mother’s undernutrition have a severe impact on
their babies weight, besides other pathologies such as allergies, asthma an other
health problems. Studies on pregnant mothers that suffered from the Dutch Famine
during the last years of the war had underweight children; their granddaughters
suffered also of reduced fetal growth, albeit their mothers not having experienced the
severe restrictive diets they grandmothers had (Susser and Stein, 1994). It seems
likely that epigenetic markings explain these family crossgenerational effects
notwithstanding their differential environmental exposures (Lumey, 1992; Roseboom
et al., 2001). Epigenetic crossgenerational effects of famine due to war conditions
have been reported for other European countries as well (Van Den Berg et al., 2011)

Trauma, violence and abuse should also be taken into account. The placental
environment protects the foetus up to a certain limit from their pregnant mothers’
production of cortisol when suffering from stress or anxiety. But maternal cortisol
production during pregnancy after severe post-traumatic stress predicts high levels of
cortisol in the second and also in the third generations. This alteration of stress
reactivity has been reported in pregnant mothers who were survivors of the Holocaust
and their grandchildren. Similarly, offspring of gestating mothers exposed to the 9/11
attack in Manhattan gave birth to babies with hypothalamic-pituitary-adrenal axis
alterations as well as stress response disorders in early childhood (Yehuda and Bierer,
2008). It has been suggested that many of these uterine experiences induce specific
types of responsiveness due the triggering of epigenetic changes in the foetus.

X.5. Racialised becomings

X.5.1. Political economy of health, suffering and social exclusion

Different forms of power, socioeconomic organisation and classificatory systems

produce specific group and individual experiential environments. The
disenfranchisement of huge parts of the population (Lende, 2008) increase their
exposure to vulnerability and health risk.
Endocrinologist Robert Sapolsky (2004) says that, since social species show
social hierarchies and ranks, social status has a strong influence on the quality of life
of group members. In humans, economic deprivation, undernutrition, poor housing
conditions, education and medical access, exposure to pollution and toxics, lack of
education, little access to medical facilities, diseases, epidemics, and catastrophes,
discrimination, exploitation, violence and abuse, suffering 27 have direct consequences

27
Leisure activities, as part of a (socioculturally and historically defined) pleasant life influence
endorphine production, contributing to wellbeing and stronger self-defence against infections, which, in
turn, contributes to a better and longer life (Hyyppä et al., 2006).
16
for people’s life expectancy and health. Low social status has been correlated with
psychoemotional stress and cell metabolism and oxidation (aging), reducing life
expectancy through telomere shortening after successive chromosome replication
(Cherkas et al., 2006). Also with a depressed immune system, cardiovascular
suffering, and possible reproductive cycle changes.

Occupational and work-related diseases and deformities are well-known in

historical demography. There are strong links between bones, culture and activity
(Fausto-Sterling, 2005, 2008). Ethnic devaluation, income and health are strongly
connected in some populations (Walls and Williams, 2004). Many wolrd infectious
diseases follow the same distribution of malnutrition and poverty.

There is no doubt that we can speak of a political economy of health, suffering

and risk exposure (Goodman et al., 2005).

X.5.2. Genes, race and the metabolic syndrome

Globesity, a term recently introduced by the World Health Organisation,

concerns the global epidemics that is becoming a national health crisis in the USA
(Ford et al., 2002), as in many other developed countries and emergent economies.
Obesity is part of the metabolic syndrome, which also include hypertension28 and
insulin resistance. It is a precursor of stroke and coronary heart disease, hence, of
premature death associated with these conditions29.
In the USA, statistics show that so-called African Americans (AA) suffer twice as
much from this syndrome compared to so-called White American (WA). Mortality due
to these health problems is much higher in the fist group than in the second (Mensah
et al., 2005; Nesbitt and Victor, 2004).
Some epidemiologists have tried to establish a causal connection between the
prevalence of this syndrome and genetic hereditary factors of race30. But genetic
diversity has nothing to do with racial categorisations (Armelagos and Goodman,
1998), which are politically and historically constructed essentialist classifications for
discrimination and segregation based on irrelevant phenotypic differences 31. Even so,
this does not seem the case. Race cannot be a legitimate scientific explanation for any
genetic variability, neither for empirical health disparities (Goodman, 2000).
If race is not the reason for this heterogeneity between Afro-Americans and
White-Americans, it must be sought elsewhere. It is true that hypercaloric diets,
sedentary life and brown adipose tissue that transfer energy from food into heat are

28
Especially in African American women, but not in West Indies AfroAmericans, irrespectively of sex
difference. Neither for Africans (Cooper et al., 1997).
29
Waist circumference has become a good risk predictor of obesity associated problems.
30
In 2015, the American Food and Drug Administration approved the first race(ial)-specific
pharmaceutical to treat heart failure in so-called African-Americans, opening up a new market for
pharma-industries interested in a new possibility of medical customization and commodification: racial
differences. The geneticisation of race in medical research is becoming a serious challenge both to
science and to non-discriminatory policies and ideologies (Pálsson, 2007).
31
If clusters of genetic similarity can be found in some populations, they do not correspond to racial
partitioning but, in any case, to their probable geographical areas of origin (Templeton, 1998).
17
important factors in obesity32, but this cannot explain why it is that people with similar
life-styles show such a disparity.

X.5.3. Physiological stress, pre-natal developmental niches and birth differences

Neither prematurity nor body weight when born are genetic. One of the most
relevant consequences of nutritional insult in the gestating mother, together with
emotional stress during pregnancy, is giving birth to premature or low weight babies.
Nutrition and diet are important factors in mammals’ developmental
environments. Mammal studies have given evidence of the relations between
malnutrition, lack of necessary proteins and nutrients, and placental size, with lifelong
changes in the body and its systems, including mental and psychological disorders in
later life (Antonow-Schlorke et al., 2011). Deprivation of the caring environment of
the placenta because of premature birth (cf. (Bainbridge, 2003), has been correlated
with organic and functional underdevelopment in foetus brain and lung tissue, plus
the high probability of medicalisation in baby’s and infant’s early ontogeny, if not all
through the course life33.
Pre-term or low weight babies exposed later in life to rich caloric diets – i.e.
cheap junk food - are not biologically prepared for such quick a metabolic change.
They tend to show a higher propensity to weight gain, metabolic glucose and lipid
disorders, precursors of later cardiovascular diseases. It is as if as if they were
already able to make the most of their diet in a context of food shortage when born,
as if their metabolic threshold for coping with a caloric diet without major health
consequences would be lower than that of full-term/normal weight babies. This
mismatch between pre-perinatal environments and those of childhood, youth and
adulthood may explain the prevalence of future obesity and its correlated diseases.

Let us go back to the health differences in USA mentioned before. So-called

African-American mothers tend to give birth to underweight babies, twice as often as
Euro-American mothers, either pre- or full-term34. But this was not the case for
African-born mothers giving birth in USA, who had full term normal weight babies 35.
In contrast, their Afro-American born daughters, entering a similar niche of social
exclusion as pre-natal environments for development, will progressively tend to
deliver premature and/or low birth weight babies (Kuzawa and Sweet, 2009).
The prevalent life environment of many Afro-American pregnant mothers are
very much those of malnutrition, unhealthy lifestyles and precarious living conditions,
limited access to prenatal and postnatal medical care, and strong psycho-emotional
stress (depression, anxiety, overwork, single motherhood). It is the influence of the
mother’s embodied specific responsiveness to environmental distress and hardship,
linked to the effects of social exclusion and discrimination practices within a racist
political economy, and with her personal psychoemotional experiences and home
32
Abdominal adipocytes are big white fat cells, the main producers of cytokines, which are directly
related to the endocanabinoid system, the deposition of lipids in the arteries and inflammatory
processes (López-Jaramillo et al., 2005).
33
Less conspicuous changes refer to organ size, cell number, type and number of body fat cells,
producers of cytokines, which are linked to inflammatory processes.

34
In discussing this we will follow the illuminating work of Cristopher W. Kuzawa and Elizabeth Sweet
(Kuzawa and Sweet, 2009).
35
Neither for Euro-American mothers.
18
atmosphere, that produce specific developmental niches for children that may
increase their future risk of suffering from the metabolic syndrome, that explain
better the health differences found so-called African-American groups and so-called
Americans from European origins.

X.5.4. Racism and matrilineal cycles of social exclusion

We know that embryo and foetus embodied responsiveness to uterine specific

environments, in the form of epigenetic changes, can be imprinted in the child’s
gamete, and passed later to his/her children, and through them, to future
generations. Kuzawa and Sweet (2009) suggest that the chronic effects of social-
environmental exposures, epigenetic conditions maintained, go well beyond the
generations into the following ones and even their offspring.
Developing health problems jeopardize social and economic opportunities both
at the person and the group level, triggering a repetitive self-induced life cycles of
bad health and social exclusion. This ontogenetic loop may be re-enacted in the
offspring’s local biology, and passed to their future generations through the germ line.

It is the complex stochastic embodiment of multiple interactive systems of life-

in-the-making of a) socio-political, economical and ideological discriminatory
structures and practices, b) together with individual and biographical experiences, c)
which produce certain maternal physiological and psychological responsiveness that
constitute the child’s pre, peri – and post natal environments, c) that
produce/maintain specific epigenetic states, d) that, in turn, may be passed as
epigenetic marks unto future generations, that we may speak of matrilineal family
cycles of biosocial suffering and exclusion in racial(ised) groups.
These crossgenerational maternal effects may contribute to the perpetuation of
social structure’s cleavages and social exclusion through time. Individual live courses
of unhealthy life styles that again depend on income, social status, but also on
socialisation in group traditions and values, may reinforce these matrilineal epigenetic
phylogenies of differing biosocial becomings.

CONCLUSIONS

This paper started with a critical review of the gene-centered view of human
phenotype and behaviour. We claimed the relevance of epigenetic processes within an
epistemological shift towards developmental systems in the construction of life and
phenotypes. We then emphasised the relevance of human material-symbolic
productions in the construction of developmental niches. From that, we tried to
connect these niches with health and a political economy of inequality and deprivation
of some populations. Then we explained the cross-generational effects of epigenetic
changes, both in ontogeny and through the germ line. Within a biopsicosociocultural
and political framework, we were able to argue for a racialised material-symbolic
explanation of human becomings, not by genetic factors. We wanted to show the
transcendence of our practices, representations and discourses beyond their
generational temporality, and how social doings and makings are bioculturally and
politically reproduced in cross-generational cycles of social exclusion and
discrimination. In doing this, we have tried to put together our two main areas of
19
research: alterity, social exclusion and ethnicity, and a biopsisociocultural and
historico-political interdisciplinary approach to human affairs.
Some of the conclusions we may draw from this paper are the following.
Epigenesis is a core factor in the post-genomic shift from genetic determinism
to interactional networks of stochastic genomic processes in
developmental/developing environments. This shift is fundamental for a
biopsicosociocultural approach to human becomings and how life is a process in-the-
making.
Political, economical, ideological, historical and biographical factors are
embodied by pregnant mothers, influencing their child developmental niches, which in
turn produce specific epigenetic states, with probable health consequences during the
life-course, impinging on people’s socioeconomic careers and status.
Parental and ancestors epigenetic marks may transcend the generational cohort in
which they took place, crossing over to following and future generations, establishing
a propensity to suffer some health conditions.
If the genome was not our destiny, neither it is our epigenome. Although
epigenetic marks can be passed without experiencing the life conditions that once
triggered them, especially attention may be paid in reversing their effects. We are
the repositories of our genome/epigenome legacy not only for us, but also for our
descendants and their future progeny, which involves ethical and political decisions of
how we decide - or are allowed – to carry out our present lives.
This is not only a personal responsibility, but a collective one. Proper interventions
during the life course, especially in crucial human developmental stages such as the
embryo, foetus, infancy, childhood and adolescence, can counteract the negative
biological effects of embodied political economies of inequality in human becomings.
Public policies should focus on socioeconomically and politically induced life styles that
produce biochemical, hormonal, and neuropsychological predispositions of unequal
human developments. The transformation and improvement of developmental niches
and long-life environments for young people, adults and the elderly are possible,
provided that a political commitment exists and the necessary resources are
allocated36.

Last but not least, the political economy, historicity, and socioculturality, of human
epigenetic landscapes and their possible crossgenerational perpetuation open up a
promising scenario for real interdisciplinary collaboration between the life sciences
and the social sciences, contributing to a very much needed eradication of dualistic
thinking.

References

36
Effects of unbalanced nutrition and health correlates can be reversed at some point. With a three-
month Mediterranean diet based on cereals, fish, olive oil and some wine, these markers change
drastically (Estruch and Al., 2006); also, prostate cancer patients who showed intolerance to
chemotherapy could control oncogen expression by means of a hypocaloric diet, one and a half hours
exercise each day and daily meditation (Barnard et al., 2008). See also The Southampton Initiative for
Health (SIH), a clinical and social intervention to improve the health life styles of women and their
offspring in Southhampton (UK), at http://www.mrc.soton.ac.uk/index.asp?page=291

20
21