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Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? Surely Roberts would agree that we use her socio-political concept of race when it comes to medicine, but not treat them like biological races. Roberts is an anti-realist about biological races, whereas Hardimon is not—he recognizes that there is a minimalist and social aspect to race which are separate concepts.
In his book Rethinking Race: The Case for Deflationary Realism, Hardimon (2017, Chapter 8) discusses race and medicine after discussing and defending his different race concepts. If race is real—whether socially, biologically, or both—then why should we ignore it when it comes to medical contexts? It seems to me that many people would be hurt by such a denial of reality, and that’s what most people want to prevent, and which is the main reason why they deny that races exist, so it seems counterintuitive to me.
Hardimon (2017: 161-162; emphasis his) writes:
If, as seems to be the case, the study of medically relevant genetic variants among races is a legitamate project, then exclusionism about biological race in medical research—the view that there is no place for a biological concept of race in medical research—is false. There is a place for a biological concept of race in the study of medically relevant genetic variants among races. Inclusionism about biological race in medical research is true.
So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). Sure, some critics would argue that we should be looking at the individual and not their racial or ethnic group. But consider this: Imagine that an individual has something wrong and standard tests do not find out what it is. The doctor then decides that the patient has X disease. They then treat X disease, and then find out that they have Y disease that a certain ethnic group is more likely to have. In this case, accepting the reality of biological races and its usefulness in medical research would have caught this disease earlier and the patient would have gotten the help they needed much, much sooner.
Black women are more likely to die from breast cancer, for example, and racism seems like it can explain a lot of it. They have less access to screening, treatment, care, they receive delays in diagnoses, along with lower-quality treatment than white women. But “implicit racial bias and institutional racism probably play an important role in the explanation of this difficult treatment” (Hardimon, 2017: 166). Furthermore, black women are more than twice as likely to acquire a type of breast cancer called “triple negative” breast cancer (Stark et al, 2010; Howlader et al, 2014; Kohler et al, 2015; DeSantis et al, 2019). Of course, this could be a relevant race-related genetic difference in disease.
We should, of course, use the concepts of socialrace when discussing the medical effects of racism (i.e., psychosocial stress) and the minimalist/populationist race concepts when discussing the medically relevant race-related genetic diseases. Being eliminativist about race doesn’t make sense—since if we deny that race exists at all and do not use the term at all anymore, there would be higher mortality for these “populations.” Thus, we should use both of Hardimon’s terms in regard to medicine and racial differences in health outcomes as both concepts can and will show us how and why diseases are more likely to appear in certain racial groups; we should not be eliminativists/exclusionists about race, we should be inclusionists.
Hardimon discusses how racism can manifest itself as health differences, and how this can have epigenetic effects. He writes (pg 155-156):
As philosopher Shannon Sullivan explains, another way in which racism may be shown to influence health is by causing epigenetic changes in the genotype. It is known that changes in gene expression can have durable and even transgenerational effects on health, passing from parents to their children and their children’s children. This suggests that the biological dimensions of racism can replicate themselves across more than one generation through epigenetic mechanisms. Epigenetics, the scientific study of such changes, explains how the process of transgenerational biological replication of ill health can occur without changes in the underlying DNA sequence.
If such changes to the DNA sequences can be transmitted to the next generation in the developmental system, then that means that the social can—and does—has an effect on our biology and that it can be passed down through subsequent generations. It is simple to explain why this makes sense: for if the developing organism was not plastic, and genes could not change based on what occurs in the environment for the fetus or the organism itself, then how could organisms survive when the environment changes if the “genetic code” of the genome were fixed and not malleable? For example, Jasienska (2009) argues that:
… the low birth weight of contemporary African Americans not only results from the difference in present exposure to lifestyle factors known to affect fetal development but also from conditions experienced during the period of slavery. Slaves had poor nutritional status during all stages of life because of the inadequate dietary intake accompanied by high energetic costs of physical work and infectious diseases. The concept of ‘‘fetal programming’’ suggests that physiology and metabolism including growth and fat accumulation of the developing fetus, and, thus its birth weight, depend on intergenerational signal of environmental quality passed through generations of matrilinear ancestors.
If the environmental quality—i.e., current environmental quality—is “known” by the developing fetus through cues from the mother’s nutrition, stress etc, then a smaller body size may be adaptive in that certain environment and the organism may survive with fewer resources due to smaller body size. In any case, I will discuss this in the future but it was just an example of a possible epigenetic modification on current slaves. I, personally, have noticed that a lot of blacks are really skinny and have really low body fat—who knows, maybe this could be part of the reason why?
This is something that sociologist Maurizio Meloni (2018) calls “the postgenomic body”—the fact that biology is malleable through what occurs in our social lives. So not only is the human brain plastic, but so is the epigenome and microbiome, which is affected by diet and lifestyle—along with what we do and what occurs to us in our social lives. So our social lives, in effect, can become embodied in our epigenome and passed down to subsequent generations. Similar points are also argued by Ulijaszek, Mann, and Elton (2012). (Also see my article Nutrition, Development, Epigenetics, and Physical Plasticity.)So in effect, environments are inherited too, and so, therefore, the environments that we find ourselves in are, in effect, passed down through the generations. Meloni (2018) writes:
On the other hand, by re-embedding the individual within a wider lineage of ancestral experiences and reconfiguring it as a holobiontic assemblage, it may literally dissolve the subject of emancipation. Moreover, the power of biological heredity may be so expanded (as it includes potentially any single ancestral experience) to become stronger than in any previous genetic view. Finally, the several iterations of plasticity that emerge from this genealogy appear so deeply racialized and gendered that it is difficult to quickly turn them into an inherently emancipatory concept. Even as a concept, plasticity has an inertial weight and viscosity that is the task of the genealogist to excavate and bring into view.
Thus, current biological states can be “tagged” and therefore be epigenetically transmitted to future generations. Think about it in this way: if epigenetic tags can be transmitted to the next generation then it would be presumed that that environment—or a similar one—would be what newer generations would be born in. Thus, the plasticity of the organism would help it in life, especially the immediate plasticity of the organism in the womb. Likewise, Kuzawa and Sweet (2008) argue:
that environmentally responsive phenotypic plasticity, in combination with the better-studied acute and chronic effects of social-environmental exposures, provides a more parsimonious explanation than genetics for the persistence of CVD disparities between members of socially imposed racial categories.
Of course, if we look at race as both a biological and social category (i.e., Spencer, 2014), then this is not surprising that differences in disease acquisition can persist “between members of socially imposed racial categories.” Phenotypic plasticity is the big thing here, as noted by many authors who write about epigenetics. If the organism is plastic (if it can be malleable and change depending on external environmental cues), then disease states can—theoretically—be epigenetically passed to future generations. This is just like Jasienska’s (2009, 2013, Chapter 5) argument that the organism—in this case, the fetus—can respond to the environmental quality that it is developing in and, therefore, differences in anatomy and physiology can and do occur based on the plasticity of the organism.
Lastly, Jan Badke, author of Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics (Baedke, 2018), argues that, since the gene-centered view of biology has been upended (i.e., Jablonka and Lamb, 2005; Noble, 2006, 2011, 2012, 2017) for a postgenomic view (Richardson and Stevens, 2015). Genes are not closed off from the environment; all organisms, including humans, are open systems and so, there are relationships between the environment, developmental system, and the genome which affect the developing organism. Baedke and Delgado (2019) argue that the “colonial shadow … biologicizes as well as racializes social-cultural differences among human groups.” Since every race faces specific life challenges in its environment, therefore, each race shows a “unique social status that is closely linked to its biological status.” Thus, differing environments, such as access to different foods (i.e., the effects of obesifying foods) and discrimination can and are passed down epigenetically. Baedke and Delgado (2019: 9) argue that:
… both racial frameworks nutrition plays a crucial role. It is a key pathway over which sociocultural and environmental difference are embodied as racial difference. Thus, belonging to a particular race means having a particular biosocial status, since races include two poles – a social status (e.g., class, socio-economic status) and a biological status (disease susceptibility) – which are closely interlinked. Against this background, human populations in Mexico become an exemplar of types of bodies that are not only relocated to a destabilizing modernized world in which they suffer from socio-economic deprivation. What is more, they become paradigmatic primitive bodies that are unbalanced, biologically deprived, and sick. In short, in these recent epigenetic studies poor places and lifestyles determine poor bodies, and vice versa.
In sum, accepting the reality of race—both in a minimalist/populationist biological manner and social manner—can and will help us better understand disease acquisition and differing levels of certain diseases between races. Recognizing the minimalist/populationist concepts of race will allow us to discover genetic differences between races that contribute to variation in different diseases—since genes do not alone outright cause diseases (Kampourakis, 2017: 19). Being eliminativist/exclusionist about race does not make sense, and it would cause much more harm than good when it comes to racial disease acquisition and mortality rates.
Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the “oppression” is imagined, it can still have very real biological effects that could be passed onto the next generation—and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies; these effects also could have possibly manifested itself in regard to obesity in Latin America post-colonialism. Gravlee (2009) and Kaplan (2010) also argue that the social, too, manifests itself in biology.
(For further information on how the social can and does become biological see Meloni’s (2019) book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics, along with Meloni (2014)‘s paper How biology became social, and what it means for social theory. Reading Baedke’s and Meloni’s arguments on plasticity and epigenetics should be required before discussing these concepts.)
Two dominant theories exist in regard to development, the “gene’s eye view—gene selectionism (GS)—and the developmental view—developmental systems theory (DST). GS proposes that there are two fundamental processes in regard to evolution: replication and interaction. Replicators (the term was coined by Dawkins) are anything that is copied into the next generation whereas interactors (vehicles) are things that only exist to ensure the replicators’ survival. Thus, Dawkins (1976) proposes a distinction between the “vehicle” (organism) and its “riders/replicators” (the genes).
Gene selectionists propose a simple hypothesis: evolution through the differential survival of genes, its main premise being that the “gene” is “the ultimate, fundamental unit of natural selection.” Dusek (1999: 156) writes that “Gene selection claims that genes, not organisms, groups of organisms or species, are selected. The gene is considered to be the unit of selection.” The view of gene selectionists is best—and most popularly put—by Richard Dawkins’ seminal book The Selfish Gene (1976), in which he posits that genes “compete” with each other, and that our “selfish actions” are the result of our genes attempting to replicate to the next generation, relegating our bodies to disposable “vehicles” that only house the “replicators” (or “drivers).
Though, just because one is a gene selectionist does not necessarily mean that they are a genetic determinist (both views will be argued below). Gene selectionists are comitted to the view that genes make a distinctive contribution toward building interactors. Dawkins (1982) claims that genetic determinism is not a problem in regard to gene selectionism. Replicators (genes) have a special status to gene selectionists. Gene selectionists argue that adaptive evolution only occurs through cumulative selection, while only the replicators persist through the generations. Gene selectionists do not see organisms as replicators since genes—and not organisms—are what is replicated according to the view.
The gene selectionist view (Dawkins’ 1976 view) can also be said to apply what Okasha (2018) terms “agential thinking”. “Agential thinking” is “treating an evolved organism as if it were an agent pursuing a goal, such as survival or reproduction, and treating its phenotypic traits, including its behaviour, as strategies for achieving that goal, or furthering its biological interests” (Okasha, 2018: 12). Dawkins—and other gene selectionists—treat genes as if they have agency, speaking of “intra-genomic conflict”, as if genes are competing with each other (sure, it’s “just a metaphor”, see below).
Okasha (2018: 71) writes:
To see how this distinction relates to agential thinking, note that every gene is necessarily playing a zero-sum game against other alleles at the same locus: it can only spread in the population if they decline. Therefore every gene, including outlaws, can be thought of as ‘trying’ to outcompete alleles, or having this as its ultimate goal.
Selfish genes also have intermediate goals, which are to maximize fitness, which is done through expression in the organismic phenotype.
Thus, according to Okasha (2018: 73), “… selfish genetic elements have phenotypic effects which can be regarded as adaptations, but only if we apply the notions of agent, benefit, and goal to genes themselves”, though “… only in an evolutionary context [does] it [make] sense to treat genes as agent-like and credit them with goals and interests.” It does not “make sense to treat genes as even “agent-like and credit them with goals and interests since they can only be attributed to humans.
Other genes have as their intermediate goal to enhance the fitness of their host organism’s relatives, by causing altruistic behaviour [genes can’t cause altruistic behavior; it is an action]. However, a small handful of genes have a different intermediate goal, namely to increase their own transmission in their host organism’s gametes, for example, by biasing segregation in their favour, or distorting the sex-ratio, or transposing to new sites in the genome. These are outlaws, or selfish genetic elements.If oulaws are absent or are effectively suppressed, then the genes within a single organism have a common (intermediate) goal, so will cooperate: each gene can onluy benefit by itself by benefiting the whole organism. Agential thinking then can be applied to the organism itself. The organism’s goal—maximizing its fitness—then equates to the intermediate goal of each of the genes within it. (Okasha, 2018: 72)
Attributing agential thinking to anything other than humans is erroneous, since genes are not “selfish.”
The selfish gene is one of the main theories that define the neo-Darwinian paradigm and it is flat out wrong. Genes are not ultimate causes, as the crafters of the neo-Darwinian Modern Synthesis (MS) propose, genes are resources in a dynamic system and can thusly only be seen as causes in a passive, not active, sense (Noble, 2011).
The alternative to the gene-centric view of evolution is that of developmental systems theory (DST), first proposed by Oyama (1985).
The argument for DST is simple:
(1) Organisms obviously inherit more than DNA from their parents. Since organisms can behave in ways that alter the environment, environments are also passed onto offspring. Thus, it can be said that genes are not the only things inherited, but a whole developmental matrix is.
(2) Genes, according to the orthodox view of the MS, interact with many other factors for development to occur, and so genes are not the only thing that help ‘build’ the organism. Genes can still play some “privileged” role in development, in that they “control”, “direct” or “organize” everything else, but this is up to gene-selectionists to prove. (See Noble, 2012.)
(3) The common claim that genes contain “information” (that is, context-independent information) is untenable, since every reconstruction of genes contain development about information applies directly to all other developmental outcomes. Genes cannot be singled out as privileged causes in development.
(4) Other attempts—such as genes are copied more “directly—are mistaken, since they draw a distinction between development and other factors but fail.
(5) Genes, then, cannot be privileged in development, and are no different than any other developmental factor. Genes, in fact, are just passive templates for protein construction, waiting to be used by the system in a context-dependent fashion (see Moore, 2002; Schneider, 2007). The entire developmental system reconstructs itself “through numerous independent causal pathways” (Sterelny and Griffiths, 1999: 109).
DNA is not the only thing inherited, and the so-called “famed immortality of DNA is actually a property of cells [since] [o]nly cells have the machinery to correct frequent faults that occur in DNA replication.” The thing about replication, though, is that “DNA and the cell must replicate together” (Noble, 2017: 238). A whole slew of developmental tools are inherited and that is what constructs the organism; organisms are, quite obviously, constructed not by genes alone.
Developmental systems, as described by Oyama (1985: 49) do not “have a final form, encoded before its starting point and realized at maturity. It has, if one focuses finely enough, as many forms as time has segments.” Oyama (1985: 61) further writes that “The function of the gene or any other influence can be understood only in relation to the system in which they are involved. The biological relevance or any influence, and therefore the very “information” it conveys, is jointly determined, frequently in a statistically interactive, not additive, manner, by that influence and the system state it influences.”
DNA is, of course, important. For without it, there would be nothing for the cell to read (recall how the genome is an organ of the cell) and so no development would occur. DNA is only “information” about an organism only in the process of cellular functioning.
The simple fact of the matter is this: the development of organs and tissues are not directly “controlled” by genes, but by the exchange signals of the cells. “Details notwithstanding, what is important to note is that whatever kinds of signals it sends out depends on the kind of signals it receives from its immediate environment. Therefore, neighboring cells are interdependent, and its local interactions among cells that drive the developmental processes” (Kampourakis, 2017: 173).
The fact of the matter is that whether or not a trait is realized depends on the developmental processes (and the physiologic system itself) and the environment. Kampourakis, just like Noble (2006, 2012, 2017) pushes a holistic view of development and the system. Kampourakis (2017: 184) writes:
What genetics research consistently shows is that biological phenomena should be approached holistically. at various levels. For example, as genes are expressed and produce proteins, and some of these proteins regulate or affect gene expression, there is absolutely no reason to privilege genes over proteins. This is why it is important to consider developmental processes in order to undertand how characters and disease arise. Genes cannot be considered alone but only in the broader context (cellular, organismal, environmental) in which they exist. And both characters and disease in fact develop; they are not just produced. Therefore, reductionism, the idea that genes provide the ultimate explanation for characters and disease, is also wrong. In order to understand such phenomena, we need to consider influence at various levels of organization, both bottom-up and top-down. This is why current research has adopted a systems biology approach (see Noble, 2006; Voit, 2016 for accessible introductions).
All this shows that developmental processes and interactions play a major role in shaping characters. Organisms can respond to changing environments through changes in their development and eventually their phenotypes. Most interestingly, plastic responses of this kind can become stable and inherited by their offspring. Therefore, genes do not predetermine phenotypes; genes are implicated in the development of phenotypes only through their products, which depends on what else is going on within and outside cells (Jablonka, 2013). It is therefore necessary to replacr the common representation of gene function presented in Figure 9.6a, which we usually find in the public sphere, with others that consider development, such as the one in figure 9.6b. Genes do not determine characters, but they are implicated in their development. Genes are resources that provide cells with a generative plan about the development of the organism, and have a major role in this process through their products. This plan is the resouce for the production of robust developmental outcomes that are at the same time plastic enough to accomodate changes stemming from environmental signals.
Figure 9.6 (a) The common representation of gene function: a single gene determines a single phenotype. It should be clear by what has been present in the book so far that is not accurate. (b) A more accurate representation of gene function that takes development and environment into account. In this case, a phenotype is propduced in a particular environment by developmental processes in which genes are implicated. In a different environment the same genes might contribute tothe development of a different phenotype. Note the “black box” of development.
[Kampourakis also writes on page 188, note 3]
In the original analogy, Wolpert (2011, p. 11) actually uses the term “program.” However, I consider the term “plan” as more accurate and thus more appropriate. In my view, the term “program” impies instructions and their implimentation, whereas the term “plan” is about instructions only. The notion of a genetic program can be very misleading because it implies that, if it were technically feasible, it would be possible to compute an organism by reading the DNA sequence alone (see Lewontin, 2000, pp. 17-18).
Kampourakis is obviously speaking of a “plan” in a context-dependent manner since that is the only way that genes/DNA contain “information” (Moore, 2002; Schneider, 2007). The whole point is that genes, to use Noble’s terminology, are “slaves” to the system, since they are used by and for the (physiological) system. Developmental systems theory is a “wholeheartedly epigenetic approach to development, inheritance and evolution” (Hochman and Griffiths, 2015).
This point is driven home by Richardson (2017:111):
And how did genes eventually become established? Probably not at all as the original recipes, designers, and controllers of life. Instead they arose as templates for molecular components used repeatedly in the life of the cell and the organism: a kind of facility for just-in-time production of parts needed on a recurring basis. Over time, of course, the role of these parts themselves evolved to become key players in the metabolism of the call—but as part of a team, not the boss.
It is not surprising, then, that we find that variation in form and function has, for most traits, only a tenuous relationship with variation in genes.
[And also writes on page 133]:
There is no direct command line between environments and genes or between genes and phenotypes. Predictions and decisions about form and variation are made through a highly evolved dynamical system. That is why ostensibly the same environment, such as hormonal signal, can initiate a variaety of responses like growth, cell division, differentiation, and migration, depending on deeper context. This reflects more than fixes responses from fixed information in genes, something fatally overlooked in the nature-nurture debate
(Also read Richardson’s article So what is a gene?)
The gene-selectionist point-of-view entails too many (false) assumptions. The DST point of view, on the other hand, does not fall prey to the pitfalls of the gene-selectionist POV; Developmental systems theorists look at the gene, not as the ultimate causes of development—and, along with that, only changes in gene frequency driving evolutionary change—but only as products to be used by and for the system. Genes can only be looked at in terms of development, and in no other way (Kamporuakis, 2017; Noble, 2017). Thus, the gene-selectionists are wrong; the main tenet of the neo-Darwinian Modern Synthesis, gene-selectionism—the selfish gene—has been refuted (Jablonka and Lamb, 2005; Noble, 2006, 2011). The main tenets of the neo-Darwinian Modern Synthesis have been refuted, and so it is now time to replace the Modern Synthesis with a new view of evolution: one that includes the role of genes and development and the role of epigenetics on the developmental system. The gene-selectionist view champions an untenable view of the gene: that the gene is priviliged above any other developmental variables, but Noble and Kampourakis show that this is not the case, since DNA is inherited with the cell; the cell is what is “immortal” to use the language of Dawkins—not DNA itself.
A priori, there is no privileged level of causation, and this includes the gene, which so many place at the top of the hierarchy (Noble, 2012).
Humans are extremely “plastic”. “Plastic” meaning that our development can be shaped by what goes on (or does not go in) in our developmental environment along with the environment outside of the womb. Many factors drive development, and if one factor changes then part of the developmental course for the organism changes as well. Thus, environment can and does drive development, with the addition (or subtraction) of different factors. In this article, I will discuss some of the factors that drive development and physical plasticity and what can change them.
Subsistence provides food while food provides nutrition. Nutrients, then, supply our bodies with energy and promote tissue growth—among other things. However, nutrient requirements vary across and between species, while all mammals need a mixture of macronutrients (carbs, fat, protein, water, and fiber) and micronutrients (vitamins and minerals). Biological variability in nutrient requirements and “the eventual degree of metabolic function that an individual can achieve for a particular intake level is determined to a greater or lesser extent by genetic variants in enzymes controlling the absorption, uptake, distribution, retention or utilization of the nutrient” (Molloy, 2004: 156). Thus, individuals who consume the same amount of micro and macronutrients—who also have different polymorphisms in genes coding for the metabolism of any nutrient (through hormones and enzymes)—can, and do, have differing physiological responses to same vitamin intake. Thus, differences in genetic polymorphisms between individuals can—and do—lead to different disease.
Next we have phenotypic plasticity. Phenotypic plasticity, simply put, is the ability for a genome to express a different phenotype in variable environments. For instance, people born in hotter environments—no matter their race or ethnicity—develop larger pores in order to sweat more, since sweating is needed for cooling the body (Lieberman, 2015). Phenotypic plasticity can be a problem, though, in environments with numerous environmental stressors that will stress the mother and, in turn, affect the baby’s development in the womb as well affecting post-birth events. An example of this is when food availability is low and exposure to infection is high (in-utero and post-birth), and when these stressors are removed, the organism in question shows “catch-up growth”, implying that these stressors impeded the development of the organism in question.
Maternal nutritional imbalance has been found—both in animal studies and epidemiological studies—and metabolic disturbances, during critical windows of development for the organism, have both a persistent effect on the health of the organism and can be transmitted epigenetically to future generations (Gallou-Kabani and Junien, 2005). Gallou-Kabani and Junien (2005) write:
Epigenetic chromatin marks may be propagated mitotically and, in some cases, meiotically, resulting in the stable inheritance of regulatory states. Transient nutritional stimuli occurring at critical ontogenic stages may have lasting influences on the expression of various genes by interacting with epigenetic mechanisms and altering chromatin conformation and transcription factor accessibility (11).
Thus, metabolic syndrome can show transgenerational effects by way of incomplete erasure of the epigenetic factors carried by grandparents and parents. (See also Treretola et al, 2005.) Epigenetic regulation was extremely important during our evolution and especially during the development of the human organism, and is how and why we are so phenotypically plastic.
Epigenetic regulation during fetal reprogramming of the individual in preparation for the environment they expect to enter is likely to be a response to seasonal energy imbalance; changes that favour the metabolic efficiency are likely to be adaptive in such circumstances. Removal of seasonal energy stress, as has taken place in contemporary industrialized societies, may turn efficiency toward pathology. Humans thus have evolved an animal model that can respond genetically (through natural selection), phenotypically (through developmental plasticity) and epigenetically (by a balance of both). (Ulijaszek, Mann, and Elton, 2013: 19)
This seems to be a fundamental response to the human organism in-utero, responding to the lack of food in its environment and growing accordingly (low birth weight, susceptibilities to differing disease), which are still a problem for much of the developed world. Though this can be maladaptive in the developed, industrialized world, since poor early-life environments can lead to epigenetic changes which then spell out bad consequences for the low-birth-weight baby who was exposed to a slew of negative nutritional factors during conception (and post-birth).
It has already been established that nutrition can alter the genome and epigenome (Niculescu and Lupu, 2011; Niculescu, 2012; Anderson, Sant, and Dolinoy, 2012). So if differing nutritional effects can alter the genome and epigenome and these effects are transgenerationally inherited by future generations, then famines change the expression of the genome and epigenome which can then inherited by future generations if the epigenetic factors carried by the grandparents and parents are not erased (and there is mounting evidence for this claim, see Yang, Liu, and Sun, 2017).
There is evidence of phenotypic plasticity regarding the lack of nutrition when it comes to humans, in-utero, and the evidence comes from the Dutch Family Studies (see Lumey et al, 2007 for an overview of the project). Individuals who were prenatally exposed to the Dutch winter famine of 1944-45, six decades later, had less DNA methylation of the IGF2 (insulin-like growth factor 2) gene than same-sex siblings who were not exposed to the winter famine (Heijmns et al, 2008). The IGF2 gene plays an essential role of the development of the fetus before birth. The gene is highly active during fetal development, but much less so after birth. (It should be noted that the loss of imprinting on the IGF2 gene can promote prostate cancer; Fenner, 2017 and loss of imprinting on IGF2 can also promote other types of cancer as well; Livingstone, 2013).
Stein et al (2009) concluded that “famine exposure prior to conception is associated with poorer self-reported mental health and a higher level of depressive symptoms.” Tobi et al (2009) write that their data “support the hypothesis that associations between early developmental conditions and health outcomes later in life may be mediated by changes in the epigenetic information layer.” Tobi et al (2014) also show that the “Epigenetic modulation of pathways by prenatal malnutrition may promote an adverse metabolic phenotype in later life.” The prenatal—and neonatal—periods of development are of utmost importance in order for the organism to develop normally, any deviation outside of these measures can—and does—affect the genome and epigenome (Hajj et al, 2014).
Another strong example that these responses are adaptive to the organism in question is the fact that people who were exposed to nutritional imbalances in the womb showed a higher chance of becoming obese later in life (Roseboom, de Rooji, and Painter, 2006). Their study has implications for babies born in developing countries (since famines mirror, in a way, developing countries). Roseboom, de Rooji, and Painter (2006: 489) write:
This may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences for health in later life.
Roseboom, de Rooji, and Painter (2006: 490) also write:
The nutritional experience of babies who were exposed to famine in early gestation may resemble that of babies in developing countries whose mothers are undernourished in early pregnancy and receive supplementation later on, but also of babies in developed countries whose mothers suffer from severe morning sickness.
So on-going studies, such as the Dutch Famine Study, have the chance to elucidate the mechanisms of low birth weight, and it can also show us how and why those exposed to adverse conditions in the womb show so many negative symptoms which are not present in kin who were not exposed to such malnutrition in the womb. These findings also suggest that nutrition before—and after—pregnancy can play a role in disease acquisition later in life. The fact that those exposed to famines have a higher chance of becoming obese later in life (Abeleen et al, 2012; Meng et al, 2017) shows that this adaptive response of the organism in the womb was very important in our evolution; the babe exposed to low maternal nutrition in the womb can, after birth, consume enough energy to become overweight, which would have been an adaptive evolutionary response to low maternal caloric energy.
Babies who are exposed to maternal under-nutrition in the womb—when exposed to an environment with ample foodstuffs—are at heightened risk of becoming type II diabetics and acquiring metabolic syndromes (Robinson, Buchholz, and Mazurak, 2007). This seems to be an adaptive, plastic response of the organism: since nutrients/energy were in low quantity in the womb, low nutrients/energy in the womb changed the epigenome of the organism, and so when (if) the organism is exposed to an environment with ample amounts of food energy, they will then have a higher susceptibility to metabolic syndromes and weight gains, due to their uterine environment. (Diet also has an effect on brain plasticity in both animals and humans, in the womb and out of it; see Murphy, Dias, and Thuret, 2014.)
In sum, phenotypic plasticity, which is driven in part by epigenetics, was extremely important in our evolution. This epigenetic regulation that occurs in the womb prepared the individual in question to be able to respond to the energy imbalance of the environment the organism was born in. The plasticity of humans, and animals, in regard to what occurs (or does not occur) in the environment, is how we were able to survive in new environments (not ancestral to our species). Epigenetic changes that occur in the grandparental and parental generations, when not completely erased during the meiotic division of cells, can affect future generations of progeny in a negative way.
The implications of the data are clear: under-nutrition (and malnutrition) affect the genome and epigenome in ways that are inherited through the generations, which is due to the physical plasticity of the human in-utero as well as post-birth when the baby developing. These epigenetic changes then lead to the one who experienced the adverse uterine environment to have a higher chance of becoming obese later in life, which suggests that this is an adaptive response to low amounts of nutrients/caloric energy in the uterine environment.