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Page 4 of 8 Kyriazis. J Transl Genet Genom 2018;2:7. I https://doi.org/10.20517/jtgg.2018.04

administrative issues (including inadequate follow-up or discharge planning, poor relationship between
[46]
patient and provider, missed appointments, lack of health insurance, and cost) . Each of these reasons in
isolation, may not be sufficiently considered as a significant obstacle. However, these must be considered as
a whole, because in real life many such issues may affect any one specific patient. Therefore, these problems
significantly reduce the likelihood that a putative anti-aging therapy can be used appropriately by any target
patient, even in the case of a putative therapy based on genomic research.

SOCIAL GENOMICS
If we reject reductionism as a model against aging, where does this leave us? In this case, a more complex-
oriented thinking may provide some direction for future research. We know that social factors and cultural
[47]
events affect the activity of our genes . These interactions are studied by the emerging science of social
genomics which tries to clarify the effect of socially-originating challenges, information or stimuli that
[48]
may have on our biology (for example, increased expression of hundreds of gene transcripts). Cole states
that: “Systems-level capabilities emerge from groups of individual, socially sensitive genomes… and …
transcriptional biofeedback (that) empirically optimizes individual well-being in the context of the unique
genetic, geographic, historical, developmental, and social contexts… Studies of human social genomics are
now clarifying which specific types of human genes are subject to social regulation and mapping the social
signal transduction pathways that mediate these effects. The results of these analyses are shedding new light
on the molecular basis for social influences on individual heath, the genomic basis for human thriving, and
the metagenomic capabilities that emerge from networked communities of socially sensitive genomes”.

In addition, a more relevant and complex view of aging can be developed when we consider the concept
[49]
of gene-culture coevolution, a concept which is associated with the general concept of social genomics .
The gene-culture coevolution concept explains the changing interactions between genetic evolution and
[50]
cultural evolution. This is also sometimes known as dual inheritance theory . An extension of this concept
[51]
describes the effects from our increasingly technological culture upon our own biology , and at the same
time, it describes how humanity can influence the further evolution of the environment itself . In this way
[52]
it may be possible to appreciate the complex and mutually influencing interactions of each patient with the
environment, and begin to form a view which is at odds with the simplistic reductionist view that “one drug
[53]
fits all” paradigm .
Furthermore, the science of social genomics and that of molecular pathological epidemiology described
below explain many of the difficulties encountered in translating genomic research into clinical therapies.
Therefore, we identify that the general reliance on the model which sees no connection between the
physicians and the patients, is changing into a model deeming the physician, the patient and their
environment to be interactive.

MOLECULAR PATHOLOGICAL EPIDEMIOLOGY
Molecular pathological epidemiology (MPE) is an emerging discipline developed, on the whole, by Harvard-
[54]
based epidemiologist Ogino et al. . It combines epidemiology and pathology in order to study more
closely the heterogeneity and aetiology of disease, including age-related disease. The approach focuses on
studies simultaneously at a microscopic (molecular, genomic, cellular), and macroscopic (organismal and
population) level. MPE helps to develop a more inclusive view of the diverse processes that underlie disease
progression. It is important to emphasise that concepts derived from MPE assist in a better appreciation
of the influence of the environment upon genetic factors. This influence may underlie several inherently
heterogeneous interacting pathological processes which may lead to disease. This makes it very difficult, if
not impossible, to adequately predict, or even study, these multiple processes which can cause significant
variations of diseases even in similar patients.