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Directed Mutations, Epigenetics and Evolution
2400 words
A mutation can be said to be directed if it arises due to the needs of the developing organism, and they occur at higher frequencies if it is beneficial (Foster, 2000; Saier et al, 2017). If there is some sort of stress, then an adaptive mutation would occur. The existence of this kind of mechanism has been debated in the literature, but its existence spells trouble for neo-Darwinian theory, whose proponents claim that mutations are random and then “selected-for” in virtue of their contributions to fitness. Indeed, this concept challenges a core tenet of neo-Darwinism (Sarkar, 1991). I will argue that directed mutation/non-random mutation/stress-directed adaptation (DM, directed mutation for short) spells trouble for the neo-Darwinian paradigm.
The issue at hand
The possibility of DMs were argued for by Cairns, Overbaugh, and Miller (1988), where they argue that environmental pressure can cause adaptive changes to genes that would be beneficial to the organism. This then spurred a long debate about whether or not such mutations were possible (see Sarkar, 1991; Fox Keller, 1992; Brisson, 2003; Jablonka and Lamb, 2014). Although Cairns, Overbaugh, and Miller were wrong—that is, they were not dealing with mutations that were due to the environmental disturbances they posed (Jablonka and Lamb, 2014: 84)—their paper did bring up the possibility that some mutations could be a direct consequence of environmental disturbances which would then be catapulted by the homeodynamic physiology of the organism.
Saier et al (2017) state the specific issue with DM and its existence:
Recently, strong support for directed mutation has emerged, not for point mutations as independently proposed by Cairns, Hall and their collaborators, but for transposon-mediated mutations (12, 13). If accepted by the scientific community, this concept could advance (or revise) our perception of evolution, allowing increased rates of mutational change in times of need. But this concept goes against the current dogma that states that mutations occur randomly, and only the beneficial ones are selected for (14, 15). The concept of directed mutation, if established, would require the reversal of a long accepted precept.
This is similar to the concept of phenotypic plasticity. It is the phenomenon of a given genotype expressing different phenotypes due to environmental factors. This concept is basically a physiological one. When talking about how plastic a phenotype is, its relation to the physiology of the organism is paramount. We know that physiological changes are homeodynamic. That is, changes in physiology are constantly happening due to the effects of the environment the organism finds itself in. For example, acute changes in heart rate occur due to what happens in the environment, like say a predator chase it’s prey. The heart rates of both predator and prey increases as blood flow increases due to stress hormones. I will discuss phenotypic plasticity on its own in the future, but for now I will just note that genetic and environmental factors influence the plasticity of phenotypes (Ledon-Rettig and Ragsdale, 2021) and that phenotypic plasticity and development play a role in evolution (West-Eberhard, 2003, 2005; Wund, 2015
The fact of the matter is, phenotypic plasticity is directly related to the concept of directed mutation, due to DM being a largely physiological concept. I will argue that this refutes a central Darwinian premise. Namely that since directed mutations are possible, then they are not random. If they are not random, then due to what occurs during the development of an organism, a directed mutation could be adaptive. This, then, is the answer to how phenotypic traits become fixed in the genome without the need for natural selection.
Directed mutations
Sueoka (1988) showed that basically all organisms are subject to directed mutations. It has been noted by mathematicans that on a purely random mutational model, that there would not be enough time to explain all of the phenotypic diversity we see today (Wright, 2000). Doubt is placed on three principles of neo-Darwinism: mutations occur independently of the environment the organism is in (this is empirically false); mutations are due to replication errors (this is true, but not always the case) and mutation rates are constant (Brisson, 2003).
One of the main claims of the neo-Darwinian paradigm is that mutations occur at random, and the mutation is selected-for or against based on its relationship to fitness. Fodor’s argument has refuted the concept of natural selection, since “selection-for” is an intensional context and so can’t distinguish between correlated traits. However, we know now that since physiology is sensitive to the environment, and since adaptive changes to physiology would occur not only in an organism but during its development, it then follows that directed mutations would be a thing, and so they wouldn’t be random as neo-Darwinian dogma would claim.
In her review Stress-directed adaptive mutations and evolution, Wright (2004) concludes:
In nature, where cell division must often be negligible as a result of multiple adverse conditions, beneficial mutations for evolution can arise in specific response to stressors that target related genes for derepression. Specific transcription of these genes then results in localized DNA secondary structures containing unpaired bases vulnerable to mutation. Many environmental stressors can also affect supercoiling and [stress-directed mutation] directly.
But what are the mechanisms of DMs? “Mechanism” in this meaning would “refer to the circumstances affecting mutation rates” (Wright, 2000). She also defines what “random” means in neo-Darwinian parlance: “a mutation is random if it is unrelated to the metabolic function of the gene and if it occurs at a rate that is undirected by specific selective conditions of the environment.” Thus, the existence of DMs would then refute this tenet of neo-Darwinism. Two of the mechanisms of such DMs are transcriptional activation and supercoiling. Transcriptional activation (TA) can cause changes to single-stranded DNA (ssDNA) and also supercoiling (the addition of more coils onto DNA). TA can be caused by either derepression (which is a mechanism which occurs due to the absence of some molecule) or induction (the activation of an inactive gene which then becomes transcribed). Thus, knowing this, “genetic derepression may be the only mechanism by which particular environmental conditions of stress target specific regions of the genome for higher mutation rates (hypermutation)” (Wright, 2000). Such responses rely on a quick response, and this is due to the plastic phenotypes of the organism which then allow such DMs to occur. It then follows that stress-induced changes would allow organisms to survive in new environments, without a need for neo-Darwinian “mechanisms”—mainly natural selection. Thus, the biochemical mechanism for such mutations is transcriptional activation. Such stress-directed mutation could be seen as “quasi-Lamarckian” (Koonin and Wolf, 2009).
In nature, nutritional stress and associated genetic derepression must be rampant. If mutation rates can be altered by the many variables controlling specific, stress-induced transcription, one might reasonably argue that many mutations are to some extent directed as a result of the unique metabolism of every organism responding to the challenges of its environment. (Wright, 2000)
This is noted wonderfully by Jablonka and Lamb (2014: 92) in Evolution in Four Dimensions:
No longer can we think about mutation solely in terms of random failures in DNA maintenance and repair. We now know that stress conditions can affect the operation of the enzyme systems that are responsible for maintaining and repairing DNA, and parts of these systems sometimes seem to be coupled with regulatory elements that control how, how much, and where DNA is altered.
Jablonka and Lamb present solid evidence that mutations are semi-directed. Such mutations, as we have seen, are able to be induced by the environment in response to stress, which is due to our plastic, homeodynamic physiology. They discuss “four dimensions” of evolution which are DNA, epigenetic, behavioral and cultural. Their works (including their Epigenetic Inheritance and Evolution: The Lamarckian Dimension; see Jablonka and Lamb, 2015) provide solid evidence and arguments against the neo-Darwinian view of evolution. The fact of the matter is, there are multiple inheritance systems over and above DNA, which then contribute to nonrandom, directed mutations. The fact of the matter is, Lamarckism wasn’t wrong and Jablonka and Lamb have strongly argued for that conclusion. Epigenetics clearly influences evolution, and this therefore vindicates Lamarckism. Epigenetic variation can be inherited too (Jablonka and Lamb, 1989). Since phenotypic plasticity is relevant in how organisms adapt to their environment, then epigenetic mechanisms contribute to evolution (Ashe, Colot, and Oldroyd, 2021). Such changes that arise due to epigenetic mechanisms can indeed influence mutation (Meyer, 2015), and I would say—more directly—that certain epigenetic mechanisms play a part in how an adaptive, directed mutation would arise during the development of an organism. Stochastic epigenetic variation can indeed become adaptive (Feinberg and Irizarry, 2010).
Non-random mutations have been known to be pretty ubiquitous (Tsunoyama, Bellgard, and Gojobori, 2001). This has even been shown in the plant Arabidopis (Monroe et al, 2022), which shows that basically, mutations are not random (Domingues, 2023). A similar concept to DMs is blind stochasticity. Noble and Noble (2017, 2018; cf Noble, 2017) have shown that organisms harness stochastic processes in order to adapt to the environment—to harness function. A stochastic process is a state of a system that cannot be predicted even knowing the current state of said system.
Even all the way back in 1979, such changes were beginning to be noticed by evolutionists, such as Ho and Saunders (1979) who write that variations in the phenotype
are produced by interactions between the organism and the environment during development. We propose, therefore, that the intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.
The organism participates in its own evolution (as considerations from niche construction show), and “evolutionary novelties” can and do arise nonrandomly (Ho, 2010). This is completely at-odds with the neo-Darwinian paradigm. Indeed, the creators of the Modern Synthesis ignored developmental and epigenetic issues when it came to formulating their theory. Fortunately, in the new millennium, we have come to understand and appreciate how development and evolution occur and how dynamic the physiological system itself truly is.
There have been critical takes on the concept of DM (Lenski and Mittler, 2003; Charlesworth, Barton, and Charlesworth, 2017; see Noble and Shapiro, 2021 for critique), like for example Futuyama (2017) who claims that DM is “groundless.” However, James Shapiro’s (1992; 2013, 2014) concept of natural genetic engineering states that cells can restructure their genomes so this “means viewing genetic change as a coordinated cell biological process, the reorganization of discrete genomic modules, resulting in the formation of new DNA structures” (Shapiro, 1993). DNA is harnessed by and for the physiological system to carry out certain tasks. Since development is self-organizing and dynamic (Smith and Thelen, 2003; Saetzler, Sonnenschein, and Soto, 2012) and since development is spurred on by physiological processes, along with the fact that physiology is sensitive to the goings-on of the environment that the developing organism finds itself in, then it follows that mutations can and would arise due to need, which would refute claims from neo-Darwinians who claim that mutations arise due to chance and not need.
Conclusion
It is clear that mutations can be (1) adaptive and (2) environmentally-induced. Such adaptive mutations, clearly, arise due to need and not chance. If they arise due to need and not chance, then they are directed and adaptive. They are directed by the plastic physiology of the organism which constructs the phenotype in a dialectical manner, using genes as its passive products, not active causes. This is because biological causation is multi-leveled, not one-way (Noble, 2012). There is also the fact of the matter that “genetic change is far from random and often not gradual” (Noble, 2013).
As can be seen in this discussion, adaptive, directed mutations are a fact of life, and so, one more domino of neo-Darwinism has fallen. Berkley claims that “The genetic variation that occurs in a population because of mutation is random“; “mutations are random“, but as we’ve seen here, this is not the case. Through the biological process of physiology and its relationship to the ebbs and flows of the environment, the organism’s phenotype that is being constructed by the self-organizing system can respond to changes in the cellular and overall environment and thusly direct changes in the phenotype and genes which would then enhance survival due to the environmental insult.
Lamarckism has been vindicated over the past 25 or so years, and it’s due to a better understanding of epigenetic processes in evolution and in the developing organism. Since what Lamarck is known for is the claim that the environment can affect the phenotype in a heritable manner, and since we now know that DNA is not the only thing inherited but epigenetically-modified DNA sequences are too, it follows that Lamarck was right. What we need to understand development and evolution is the Extended Evolutionary Synthesis, which does make novel predictions and predictions that the neo-Darwinian paradigm doesn’t (Laland et al, 2015).
Such directed changes in the genome which are caused by the physiological system due to the plastic nature of organismal construction refute a main premise of the neo-Darwinian paradigm. This is the alternative to neo-Darwinian natural selection, as Fodor noted in his attack on neo-Darwinism:
The alternative possibility to Darwin’s is that the direction of phenotypic change is very largely determined by endogenous variables. The current literature suggests that alterations in the timing of genetically controlled developmental processes is often the endogenous variable of choice; hence the ‘devo’ in ‘evo-devo’.
Darwin got quite a bit wrong, and it’s of no fault of his own. But those who claim that Darwin discovered mechanisms or articulated the random process of mutations quite obviously need to update their thoughts in the new millennium on the basis of new information informed by systems biologists and epigeneticists. The process of the construction of organisms is dynamic and self-organizing, and this is how phenotypic traits become fixed in populations of organisms. Plasticity is in fact a major driver of evolution along with the concept of genetic assimilation, which results in the canalization of the plastic trait which then eliminates the plastic response from the environment (Sommer, 2020). Phenotypic plasticity can have adaptive traits arise, but natural selection can’t be the mechanism of evolution due to Fodor’s considerations. Development can lead to evolution, not only evolution leading to development (West-Eberhard, 2003). In fact, development in many cases precedes evolution.
The Answer to Hereditarianism is Developmental Systems Theory
4150 words
Introduction
It is claimed that genes (DNA sequences) have a special, privileged role in the development of all traits. But once we understand what genes do and their role in development, then we will understand that the role ascribed to genes by gene-selectionists and hereditarians outright fails. Indeed, the whole “nature vs nurture” debate implies that genes determine traits and that it’s possible to partition the relative contributions to traits in a genetic and environmental way. This, however, is far from reality (like heritability estimates).
DST isn’t a traditional scientific theory—it is more a theoretical perspective on developmental biology, heredity, and evolution, though it does make some general predictions (Griffiths and Hochman, 2015). But aspects of it have been used to generate novel predictions in accordance with the extended evolutionary synthesis (Laland et al, 2015).
Wilson (2018: 65) notes six themes of DST:
Joint determination by multiple causes
Development is a process of multiple interacting sources.
Context sensitivity and contingency
Development depends on the current state of the organism.
Extended inheritance
An organism inherits resources from the environment in addition to genes.
Development as a process of construction
The organism helps shape its own environment, such as the way a beaver builds a dam to raise the water level to build a lodge.
Distributed control
Idea that no single source of influence has central control over an organism’s development.
Evolution as construction
The evolution of an entire developmental system, including whole ecosystems of which organisms are parts, not just the changes of a particular being or population.
Genes (DNA sequences) as resources and outcomes
Hereditarians have a reductionist view of genes and what they do. Genes, to the hereditarian, are causes of not only development but of traits and evolution, too. However the hereditarian is sorely mistaken—there is no a priori justification for treating genes as privileged causes over and above other developmental resources (Noble, 2012). I take Noble’s argument there to mean that strong causal parity is true—where causal parity means that all developmental resources are on par with each other, with no other resource having primacy over another. They all need to “dance in tune” with the “music of life” to produce the phenotype, to borrow Noble’s (2006, 2017) analogy. Hereditarian dogma also has its basis in the neo-Darwinian Modern Synthesis. The modern synthesis has gotten causality in biology wrong. Genes are, simply put, passive, not active, causes:
Genes, as DNA sequences, do not of course form selves in any ordinary sense. The DNA molecule on its own does absolutely nothing since it reacts biochemically only to triggering signals. It cannot even initiate its own transcription or replication. … It would therefore be more correct to say that genes are not active causes; they are, rather, caused to give their information by and to the system that activates them. The only kind of causation that can be attributed to them is passive, much in the way a computer program reads and uses databases. (Noble, 2011)
These ideas, of course, are also against the claim that genes are blueprints or recipes, as Plomin (2018) claims in his most recent book (Joseph, 2022). This implies that they are context-independent; we have known for years that genes are massively context-sensitive. The line of argument that hereditarians push is that genes are context-insensitive, that is they’re context-independent. But since DNA is but one of the developmental resources the physiological system uses to create the phenotype, this claim fails. Genes are not causes on their own.
Behavioral geneticist and evolutionary psychologist J. P. Rushton (1997: 64) claims that a study shows that “genes are like blueprints or recipes providing a template for propelling development forward to some targeted endpoint.” That is, Rushton is saying that there is context-independent “information” in genes, and that genes, in essence, guide development toward a targeted endpoint. Noah Carl (2019) claims that the hereditarian hypothesis “states that these differences [in cognitive ability] are partly or substantially explained by genetics.” When he says the differences are “partly or substantially explained by genetics”, he’s talking about “cognitive ability” being caused by genes. The claim that genes cause (either partly or substantially) cognitive ability—and all traits, for that matter—fails and it fails since genes don’t do what hereditarians think they do. (Nevermind the conceptual reasons.) These claims are laughable, due to what Noble, Oyama, Moore and Jablonka and Lamb have argued. It is outright false that genes are like blueprints or recipes. Rushton’s is reductionist in a sociobiology-type way, while Plomin’s is reductionist in a behavioral genetic type way.
In The Dependent Gene, David Moore (2002: 81) talks about the context-dependency of genes:
Such contextual dependence renders untenable the simplistic belief that there are coherent, long-lived entities called “genes” that dictate instructions to cellular machinery that merely constructs the body accordingly. The common belief that genes contain context-independent “information”—and so are analogous to “blueprints” or “recipes”—is simply false.
Genes are always expressed in context and cannot be divorced from said context, like hereditarians attempt using heritability analyses. Phenotypes aren’t “in the genes”, they aren’t innate. They develop through the lifespan (Blumberg, 2018).
Causal parity and hereditarianism
Hereditarianism can be said to be a form of genetic reductionism (and mind-brain identity). The main idea of reductionism is to reduce the whole to the sum of its parts and then analyze those parts. Humans (the whole) are made up of genes (the parts), so to understand human behavior, and humans as a whole, we must then understand genes, so the story goes.
Cofnas (2020) makes several claims regarding the hereditarian hypothesis and genes:
But if we find that many of the same SNPs predict intelligence in different racial groups, a risky prediction made by the hereditarian hypothesis will have passed a crucial test.
…
But if work on the genetics and neuroscience of intelligence becomes sufficiently advanced, it may soon become possible to give a convincing causal account of how specific SNPs affect brain structures that underlie intelligence (Haier, 2017). If we can give a biological account of how genes with different distributions lead to race differences, this would essentially constitute proof of hereditarianism. As of now, there is nothing that would indicate that it is particularly unlikely that race differences will turn out to have a substantial genetic component. If this possibility cannot be ruled out scientifically, we must face the ethical question of whether we ought to pursue the truth, whatever it may be.
Haier is a reductionist of not only the gene variety but the neuro variety—he attempts to reduce “intelligence” to genes and neurology (brain physiology). I have though strongly criticized the use of fMRI neuroimaging studies regarding IQ; cognitive localizations in the brain are untenable (Uttal, 2001, 2011) and this is because mind-brain identity is false.
Cofnas asks “How can we disentangle the effects of genes and environment?” and states the the behavioral geneticist has two ways—correlations between twins and adoptees and GWAS. Unfortunately for Cofnas, twin and adoption studies show no such thing (see Ho, 2013), most importantly because the EEA is false (Joseph, 2022a, b). GWAS studies are also fatally confounded (Janssens and Joyner, 2019) and PGS doesn’t show what behavioral geneticists need it to show (Richardson, 2017, 2022). The concept of “heritability” is also a bunk notion (Moore and Shenk, 2016). (Also see below for further discussion on heritability.) At the end of the day, we can’t do what the hereditarian needs to be done for their explanations to hold any water. And this is even before we look at the causal parity between genes and other developmental resources. Quite obviously, the hereditarian hypothesis is a gene-centered view, and it is of course a reductionist view. And since it is a reductionist, gene-centered view, it is then false.
Genetic, epigenetic, and environmental factors operate as a system to form the phenotype. Since this is true, therefore, both genetic and epigenetic determinism is false (also see Wagoner and Uller, 2015). It’s false because the genes one is born with, or develops with, don’t dictate or determine anything, especially not academic achievement as hereditarian gene-hunters would so gleefully claim. And one’s early experience need not dictate an expected outcome, since development is a continuous process. Although, that does not mean that environmental maladies that one experiences during childhood won’t have lasting effects into adulthood due to possibly affecting their psychology, anatomy or physiology.
The genome is responsive, that is, it is inert before it is activated by the physiological system. When we put DNA in a petri dish, it does nothing. It does nothing because DNA cannot be said to be a separate replicator from the cell (Noble, 2018). So genes don’t do anything independent of the context they’re in; they do what they do DUE TO the context they’re in. This is like Gottlieb’s (2007) probabilistic epigenesis, where the development of an organism is due to the coaction of irreducible bidirectional biological and environmental influences. David S. Moore, in The Developing Genome: An Introduction to Behavioral Epigenetics states this succinctly:
Genes—that is, DNA segments—are always influenced by their contexts, so there is never a perfect relationship between the presence of a gene and the ultimate appearance of a phenotype. Genes do not determine who we become, because nongenetic factors play critical roles in trait development; genes do what they do at least in part because of their contexts.
What he means by “critical roles in trait development” is clear if one understands Developmental Systems Theory (DST). DST was formulated by Susan Oyama (1985) in her landmark book “The Ontogeny of Information. In the book, she argues that nature and nurture are not antagonistic to each other, they are cooperative in shaping the development of organisms. Genes do not play a unique informational role in development. Thus, nature vs. nurture is a false dichotomy—it’s nature interacting with nurture, or GxE. This interactionism between nature and nurture—genes and environment—is a direct refutation of hereditarianism. What matters is context, and the context is never independent from what is going on during development. Genes aren’t the units of selection, the developmental system is, as Oyama explains in Evolution’s Eye:
If one must have a “unit” of evolution, it would be the interactive developmental system: life cycles of organisms in their niches. Evolution would then be change in the constitution and distribution of these systems (Oyama, 2000b)
Genes are important, of course, for the construction of the organism—but so are other resources. Without genes, there would be nothing for the cell to read to initiate transcription. However, without the cellular environment, we wouldn’t have DNA. Lewontin puts this wonderfully in the introduction to the 2000 edition of Ontogeny:
There are no “gene actions” outside environments, and no “environmental actions” can occur in the absence of genes. The very status of environment as a contributing cause to the nature of an organism depends on the existence of a developing organism. Without organisms there may be a physical world, but there are no environments. In like manner no organisms exist in the abstract without environments, although there may be naked DNA molecules lying in the dust. Organisms are the nexus of external circumstances and DNA molecules that make these physical circumstances into causes of development in the first place. They become causes only at their nexus, and they cannot exist as causes except in their simultaneous action. That is the essence of Oyama’s claim that information comes into existence only in the process of Ontogeny. (2000, 15-16)
Genes aren’t causes on their own, they are resources for development. And being resources for development, they have no privileged level of causation over other developmental resources, such as “methylation patterns, membrane templates, cytoplasmic gradients, centrioles, nests, parental care, habitats, and cultures” (Griffiths and Stotz, 2018). All of these things, and more of course, need to work in concert with each other.
Indeed, this is the causal parity argument—the claim that genes aren’t special developmental resources, that they are “on par” with other developmental resources (Griffiths and Gray, 1994; Griffiths and Stotz, 2018). Gene knockout studies show that the loss of a gene can be compensated by other genes—which is known as “genetic compensation.” None of the developmental resources play a more determinative role than other resources (Noble, 2012; Gamma and Liebrenz, 2019). This causal parity, then, has implications for thinking about trait ontogeny.
The causal parity of genes and other developmental factors also implies that genes cannot constitute sufficient causal routes to traits, let alone provide complete explanations of traits. Full-blown explanations will integrate various kinds of causes across different levels of organizational hierarchy, and across the divide between the internal and the external. The impossibly broad categories of nature vs. nurture that captured the imagination of our intellectual ancestors a century ago are no longer fit for the science of today. (Gamma and Liebrenz, 2019)
Oyama (2000a 40) articulates the casual parity thesis like this:
What I am arguing for here is a view of causality that gives formative weight to all operative influences, since none is alone sufficient for the phenomenon or for any of its properties, and since variation in any or many of them may or may not bring about variation in the result, depending on the configuration of the whole.
While Griffiths and Hochman (2015) formulate it like this:
The ‘parity thesis’ is the claim that if some role is alleged to be unique to nucleic acids and to justify relegating nongenetic factors to a secondary role in explaining development, it will turn out on closer examination that this role is not unique to nucleic acids, but can be played by other factors.
Genes are necessary pre-conditions for trait development, just as the other developmental resources are necessary pre-conditions for trait development. No humans without genes—this means that genes are necessary pre-conditions. If genes then humans—this implies that genes are sufficient for human life, but they are but one part of what makes humans human, when all of the interactants are present, then the phenotype can be constructed. So all of the developmental resources interacting are sufficient.
The nature vs. nurture dichotomy can be construed in such a way that they are competing explanations. However, we now know that the dichotomy is a false one and that the third way—interactionism—is how we should understand development. Despite hereditarian protestations, DST/interactionism refutes their claims. The “information” in the genes, then, cannot explain how organisms are made, since information is constructed dialectically between the resources and the system. There are a multiplicity of causal factors that are involved in this process, and genes can’t be privileged in this process. Thus the phrase “genetic causation” isn’t a coherent concept. Moreover, DNA sequences aren’t even coherent outside of cellular context (Noble, 2008).
Griffiths and Stotz (2018) put the parity argument like this:
In The Ontogeny of Information Oyama pioneered the parity argument, or the ‘parity thesis’, concerning genetic and environmental causes in development (see also Griffiths and Gray 1994; Griffiths and Gray 2005; Griffiths and Knight 1998; Stotz 2006; Stotz and Allen 2012). Oyama relentlessly tracked down failures of parity of reasoning in earlier theorists. The same feature is accorded great significance when a gene exhibits it, only to be ignored when a non-genetic factor exhibits it. When a feature thought to explain the unique importance of genetic causes in development is found to be more widely distributed across developmental causes, it is discarded and another feature is substituted. Griffiths and Gray (1994) argued in this spirit against the idea that genes are the sole or even the main source of information in development. Other ideas associated with ‘parity’ are that the study of development does not turn on a single distinction between two classes of developmental resources, and that the distinctions useful for understanding development do not all map neatly onto the distinction between genetic and non-genetic.
Shea (2011) tries to argue that genes do have a special role, and that is to transport information. Genes are, of course, inherited, but so is every other part of the system (resources). Claiming that there is information “in the genes” is tantamount to saying that there is a special role for DNA in development. But, as I hope will be clear, this claim fails due to the nature of DNA and its role in development.
This line of argument leads to one clear conclusion—genes are followers, they are not leaders; most evolution begins with environmentally-mediated phenotypic change, and then genetic changes occur (West-Eberhard, 2003). Ho and Saunders (1979) state that variation in organisms is constructed during development due to an interaction between genetic and non-genetic factors. That is, they follow what is needed to do by the developmental system, they aren’t leading development, they are but one party in the whole symphony of development. Development can be said to be irreducible, so we cannot reduce development to genes or anything else, as all interactants need to be present for development to be carried out. Since genes are activated by other factors, it is incoherent to talk of “genetic causes.” Genes affect the phenotype only when they are expressed, and other resources, too, affect the phenotype this is, ultimately, an argument genes against as blueprints, codes, recipes, or any other kind of flowery language one can used to impute what amounts to intention to inert DNA.
Even though epigenetics invalidates all genetic reductionism (Lerner and Overton, 2017), genetic reductionist ideas still persist. They give three reasons why genetic reductionist ideas still persist despite the conceptual, methodological, and empirical refutations. (1) Use of terms like “mechanism”, “trait”, and “interaction”; (2) constantly shifting to other genes once their purported “genes for” traits didn’t workout; and (3) they “buried opponents under repetitive results” (Panofsky, quoted in Lerner and Overton, 2017). The fact of the matter is, there are so many lines of evidence and argument that refute hereditarian claims that it is clear the only reason why one would still be a hereditarian in this day and age is that they’re ignorant—that is racist.
Genes, that is, are servants, not masters, of the development of form and individual differences. Genes do serve as templates for proteins: but not under their own direction. And, as entirely passive strings of chemicals, it is logically impossible for them to initiate and steer development in any sense. (Richardson, 2016)
DST and hereditarian behavioral genetics
I would say that DST challenges three claims from hereditarian behavioral genetics (HBG hereafter):
(1) The claim that we can neatly apportion genes and environment into different causes for the ontogeny of traits;
(2) Genes are the only thing that are inherited and that genes are the unit of selection and a unique—that is, special and privileged cause over and above other resources;
(3) That genes vs environment, blank skate vs human nature, are a valid dichotomy.
(1) HBG needs to rely on the attempting to portion out causes of traits into gene and environmental causes. The heritability statistic presumes additivity, thy is, it assumes no interaction. This is patently false. Charney (2016) gives the example of schizophrenia—it is claimed that 50 percent of the heritability of schizophrenia is accounted for by 8000 genes, which means that each SNP accounts for 1/8000 of the half of the heritability. This claim is clearly false, as genetics aren’t additive, and the additivity assumption precludes the interaction of genes with genes, and environment, which create new interactive environments. Biological systems are not additive, they’re interactive. Heritability estimates, therefore, are attempts at dichotomizing what is not dichitomizable (Rose, 2005).
An approach that partitions variance into independent main effects will never resolve the debate because, by definition, it has no choice but to perpetuate it. (Goldhaber, 2012)
This approach, of course, is the approach that attempts to partition variance into G and E components. The assumption is that G and E are additive. But as DST theorists have argued for almost 40 years, they are not additive, they are interactive and so not additive, therefore heritability estimates fail on conceptual grounds (as well as many others). Heritability estimates have been—and continue to today—been at the heart of the continuance of the nature vs nurture distinction, the battle, if you will. But if we accept Oyama’s causal parity argument—and due to the reality of how genes work in the system, I see no reason why we shouldn’t—then we should reject hereditarianism. Hereditarians have no choice but to continue the false dichotomy of nature vs nurture. Their “field” depends on it. But despite the fact that the main tool for the behavioral geneticist lies on false pretenses (twin and adoption studies), they still try to show that heritability estimates are valid in explaining trait variation (Segalowitz, 1999; Taylor, 2006, 2010).
(2) More than genes are inherited. Jablonka and Lamb (2005) argue that there are four dimensions—interactants—to evolution: genetic, epigenetic, behavioral, and symbolic. They show the context-dependency of the genome, meaning that genotype does not determine phenotype. What does determine the phenotype, as can be seen from the discussion here, is the interacting of developmental resources in development. Clearly, there are many other inheritance systems other than genes. There is also the fact that the gene as popularly conceived does not exist—so it should be the end of the gene as we know it.
(3) Lastly, DST throws out the false dichotomy of genes and environment, nature and nurture. DST—in all of its forms—rejects the outright false dichotomy of nature vs nurture. They are not in a battle with each other, attempting to decide who is to be the determining factor in trait ontogeny. They interact, and this interaction is irreducible. So we can’t reduce development to genes or environment (Moore, 2016) Development isn’t predetermined, it’s probabilistic. The stability of phenotypic form isn’t found in the genes (Moore and Lickliter, 2023)
Conclusion
Genes are outcomes, not causes, of evolution and they are not causes of trait ontogeny on their own. The reality is that strong causal parity is true, so genes cannot be regarded as a special developmental resource from other resources—that is, genes are not privileged resources. Since they are not privileged resources, we need to, then, dispense with any and all concepts of development that champion genes as being the leader of the developmental process. The system is, not genes, with genes being but one of many of the interactants that shape phenotypic development.
By relying on the false narrative that genes are causes and that they cause not only our traits but our psychological traits and what we deem “good” and “bad”, we would then be trading social justice for hereditarianism (genetic reductionism).
These recommended uses of bad science reinforce fears of institutionalized racism in America and further the societal marginalization of minority groups; these implications of their recommendations are never publicly considered by those who promulgate these flawed extensions of counterfactual genetic reductionism. (Lerner, 2021)
Such [disastrous societal] applications can only rob people of life chances and destroy social justice. Because developmental science has the knowledge base to change the life course trajectories of people who are often the targets of genetic reductionist ideas, all that remains to eradicate genetic reductionism from scientific discussion is to have sufficient numbers of developmental scientists willing to proclaim loudly and convincingly that the naked truth is that the “emperor” (of genetic reductionism) has no clothes. (Lerner, 2021: 338)
Clearly, hereditarians need the nature vs nurture debate to continue so they can push their misunderstandings about genes ans psychology. However, given our richer understanding of genes and how they work, we now know that hereditarianism is untenable, and DST conceptions of the gene and development as a whole have led us to that conclusion. Lerner (2017) stated that as soon as the failure of one version of genetic reductionism is observed, another one pious up—making it like a game of whack-a-mole.
The cure to hereditarian genetic reductionism is a relational developmental systems (RDS) model. This model has its origins with Uri Bronfenbrenner’s ecological systems theory (Bronfenbrenner and Ceci, 1994; Ceci, 1996; Patel, 2011; Rosa and Tudge, 2013. Development is about the interacting and relation between the individual and environment, and this is where RDS theory comes in. Biology, physiology, culture, and history are studied to explain human development (Lerner, 2021). Hereditarian ideas cannot give us anything like what models derived from developmental systems ideas can. An organism-environment view can lead to a more fruitful, and the organism and environment are inseparable (Jarvilehto, 1998; Griffiths and Gray, 2002). And it is for these reasons, including many, many more, that hereditarian genetic reductionist ideas should become mere sand in the wind.
Having said all that, here’s the argument:
P1: If hereditarianism is true, then strong causal parity is false.
P2: Strong causal parity is true.
C: Therefore hereditarianism must be false.
Evolutionary Psychology Does Not Explain Differences Between Rightists and Leftists
2000 words
Unless you’ve been living under a rock since the new year, you have heard of the “coup attempt” at the Capitol building on Wednesday, January 6th. Upset at the fact that the election was “stolen” from Trump, his supporters showed up at the building and rushed it, causing mass chaos. But, why did they do this? Why the violence when they did not get their way in a fair election? Well, Michael Ryan, author of The Genetics of Political Behavior: How Evolutionary Psychology Explains Ideology (2020) has the answer—what he terms “rightists” and “leftists” evolved at two different times in our evolutionary history which, then, explains the trait differences between the two political parties. This article will review part of the book—the evolutionary sections (chapters 1-3).
EP and ideology
Explaining why individuals who call themselves “rightists and leftists” behave and act differently than the other is Ryan’s goal. He argues, at length, that the two parties have two different personality profiles. This, he claims, is due to the fact that the ancestors of rightists and leftists evolved at two different times in human history. He calls this “Trump Island” and “Obama Island”—apt names, especially due to what occurred last week. Ryan claims that what makes Trump different from, say, Obama, is that his ancestors evolved at a different place in a different time compared to Obama’s ancestors. He further claims using the Stanford Prison Experiment that “we may not all be capable of becoming Nazis, after all. Just some, and conservatives especially so” (pg 12).
In the first chapter he begins with the usual adaptationism that Evolutionary Psychologists use. Reading between the lines in his implicit claims, he is arguing that “rightists and leftists” are natural kinds—that is, they are *two different kinds of people.* He explains some personality differences between rightists and leftists and then says that such trait differences are “rooted in biology and governed by genes” (pg 17). Ryan then makes a strong adaptationist claim—that traits are due to adaptation to the environment (pg 17). What makes you and I different from Trump, he claims, is that our ancestors and his ancestors evolved in different places at different times where different traits would be imperative to survival. So, over time, different traits got selected-for in these two populations leading to the trait differences we see today. So each environment led to the fixation of different adaptive traits which explains the differences we see today between the two parties, he claims.
Ryan then shifts from the evolution of personality differences to… The evolution of the beaks of Darwin’s finches and Tibetan adaptation to high-altitude living (pg 18), as if the evolution of physical traits is anything like the evolution of psychological traits. His folly is assuming that these physical traits can then be likened to personality/mental traits. The ancestors of rightists and leftists, like Darwin’s finches Ryan claims, evolved on different islands in different moments of evolutionary time. They evolved different brains and different adaptive behaviors on the basis of the evolution of those different brains. Trump’s ancestors were authoritarian, and this island occurred early in human history “which accounts for why Trump’s behavior seems so archaic at times” (pg 18).
The different traits that leftists show in comparison to rightists is due to the fact that their island came at a different point in evolutionary time—it was not recent in comparison to the so-called archaic dominance behavior portrayed by Trump and other rightists. Ryan says that Obama Island was more crowded than Trump Island where, instead of scowling, they smiled which “forges links with others and fosters reciprocity” (pg 19). So due to environmental adversity, they had a more densely populated “island”—in this novel situation, compared to the more “archaic” earlier time—the small bands needed to cooperate, rather than fight with each other, to survive. So this, according to Ryan, explains why studies show more smiling behavior in leftists compared to rightists.
Some of our ancestors evolved traits such as cooperativeness the aided the survival of all even though not everyone acquired the trait … Eventually a new genotype or subpopulation emerged. Leftist traits became a permanent feature of our genome—in some at least. (pg 19-20)
So the argument goes: Differences between rightists and leftists show us that the two did not evolve at the same points in time since they show different traits today. Different traits were adaptive at different points in time, some more archaic, some more modern. Since Trump Island came first in our evolutionary history, those whose ancestors evolved there show more archaic behavior. Since Obama Island came first, they show newer, more modern behaviors. Due to environmental uncertainty, those on Obama Island had to cooperate with each other. The trait differences between these two subpopulations were selected for in their environment that they evolved in, which is why they are different today. Now today, this led to the “arguing over the future direction of our species. This is the origin of human politics” (pg 20).
Models of evolution
Ryan then discusses four models of evolution: (1) the standard model, where “natural selection” is the main driver of evolutionary change; (2) epigenetic models like Jablonka’s and Lamb’s (2005) in Evolution in Four Dimensions; (3) where behavioral changes change genes; and (4) where organisms have phenotypic plasticity and is a way for the organism to respond to sudden environmental changes. “Leftists and rightists“, writes Ryan, “are distinguished by their own versions of phenotypic plasticity. They change behavior more readily than rightists in response to changing environmental signals” (pg 29-30).
In perhaps the most outlandish part of the book, Ryan articulates one of my now-favorite just-so stories. The passage is worth quoting in-full:
Our direct ancestor Homo erectus endured for two million years before going extinct 400,000 years ago when earth temperatures dropped far below the norm. Descendants of erectus survived till as recently as 14,000 years ago in Asia. The round head and shovel-shaped teeth of some Asians, including Vladimir Putin, are an erectile legacy. Archeologists believe erectus was a mix of Ted Bundy and Adolf Hitler. Surviving skulls point to a life of constant violence and routine killing. Erectile skulls are thick like a turtle’s, and the brow’s are ridged for protection from potentially fatal blows. Erectus’ life was precarious and violent. To survive, it had to evolve traits such as vigilant fearfulness, prejudice against outsiders, bonding with kin allies, callousness toward victims, and a penchant for inflexible habits of life that were known to guarantee safety. It had to be conservative. 34 Archeologists suggest that some of our most characteristic conservative emotions such as nationalism and xenophobia were forged at the time of Homo erectus. 35 (pg 33-34)
It is clear that Ryan is arguing that rightists have more erectus-like traits whereas leftists have more modern, Sapiens traits. “The contemporary coexistence of a population with more “modern” traits and a population with more “archaic” traits came into being” (pg 37). He is implicitly assuming that the two “populations” he discusses are natural kinds and with his “modern” “archaic” distinction (see Crisp and Cook 2005 who argue against a form of this distinction) he is also implying that there is a sort of “progress” to evolution.
Twin studies, it is claimed, show “one’s genetically informed psychological disposition” (Hatemi et al, 2014); they “suggest that leftists and rightists are born not made” while a so-called “consensus has emerged amongst scientists: political behavior is genetically controlled and heritable” (pg 43). But, Beckway and Morris (2008), Charney (2008), and Joseph (2009; 2013) argue that twin studies can do no such thing due to the violation of the equal environments assumption (Joseph, 2014; Joseph et al, 2015). Thus, Ryan’s claims of the “genetic origins” of political behavior rest on studies that cannot prove or disprove “genetic causation” (Shulitziner, 2017)—but since the EEA is false we must discount “genetic causation” for psychological traits, not least because it is impossible for genes to cause/influence psychological traits (see argument (iii)).
The arguments he provides are a form of inference to best explanation (IBE) (Smith, 2016). However, this is how just-so stories are created: the conclusion is already in mind, and then the story is crafted using “natural selection” to explain how a trait came to fixation and why it currently exists today. The whole book is full of such adaptive stories. Claiming that we have the current traits we do in the distributions they are in in the “populations” because they were, at a certain point in our evolutionary history, adaptive which then led to the individuals with those traits passing on more of their genes, eventually leading to trait fixation. (See Fodor and Piattelli-Palmarini, 2010).
Ryan makes such outlandish claims such as “Rightists are more likely than leftists to keep their desks neat. If in the distant past you knew exactly where the weapons were, you could find them quickly and react to danger more effectively. 26” (pg 45). He talks about how “time-consuming and effort-demanding accuracy of perception [were] more characteristic of leftist cognition … leftist cognition is more reflective” while “rightist cognition is intuitive rather than reflective” (pg 47). Rightists being more likely to endorse the status quo, he claims, is “an adaptive trait when scarce resources made energy management essential to getting by” (pg 48) Rightist language, he argues, uses more nouns since they are “more concrete, an anxious personalities prefer concrete to abstract language because it favors categorial rigidity and guarantees greater certainty” while leftists “use words that suggest anxiety, anger, threats, certainty, resistance to change, power, security, and conformity” (pg 49). There is “a connection between archaic physiology and rightist moral ideology” (pg 52). Certain traits that leftists have were “adaptive traits [that] were suited to later stage human evolution” (pg 53). Ryan just cites studies that show differences between rightists and leftists and then uses some great leaps and mental gymnastics to try to mold the findings as being due to evolution in the two different time periods he describes in chapter 1 (Trump and Obama Island).
Conclusion
I have not read one page in this book that does not have some kind of adaptive just-so story attempting to explain certain traits/behaviors between rightists and leftists in evolutionary terms. Ryan uses the same kind of “reasoning” that Evolutionary Psychologists use—have your conclusion in mind first and then craft an adaptive story to explain why the traits you see today are there. Ryan outright says that “[t]raits are the result of adaptation to the environment” (pg 17), which is a rare—strong adaptationist—claim to make.
His book ticks off all of the usual EP things: strong adaptationism, just-so storytelling, the claim that traits were selected-for due to their contribution in certain environments at different points in time. The strong adaptationist claims, for example, are where he says that erectus’ large brow “are rigid for protection from potentially fatal blows” (pg 34). Such strong adaptationist claims imply that Ryan believes that all traits are the result of adaptation and that they, as a result, are still here today because they all serve a function in our evolutionary past. His arguments are, for the most part, all evolutionary and follow the same kinds of patterns that the usual EP arguments do (see Smith, 2016 for an explication of just-so stories and what constitutes them). Due to the problems with evolutionary psychology, his adaptive claims should be ignored.
The arguments that Ryan provides are not scientific and, although they give off a veneer of being scientific by invoking “natural selection” and adaptationism, they are anything but. It is just a long-winded explanation for how and why rightists and leftists—liberals and conservatives—are different and why they cannot change, since these differences are “encoded” into our genome. The implicit claim of the book, then, that rightists and leftists are two different—natural—kinds, lies on the false bed of EP and, therefore, the arguments provided in the book fail to sway anyone that does not believe such fantastic storytelling masquerading as science. While he does discuss other evolutionary theories, such as epigenetic ones from Jablonka and Lamb (2005), the book is largely strongly adaptationist using “natural selection” to explain why we still have the traits we do in different “populations” today.
Gould, Bradbury, and Evolutionary Contingency
1800 words
I have been an avid reader and interested in astronomy/space ever since I could remember. I remember really loving Stephen Hawking and his documentaries on black holes. I would read anything I could find on constellations and stars. From there I went on to reading sci-fi. I then recall seeing The Martian Chronicles by Ray Bradbury and from then on I had become interested in sci-fi writing. But, as I grew older, I drifted away from sci-fi and now only read non-fiction. Then when I got older I got into ‘HBD’ (chronicled here) and along with it evolution—but, unlike other ‘HBDers’ I became enamored with the work of Gould, while some of my favorite books come from him. Gould wrote a lot about evolutionary contingency—the degree to which an outcome could be different. Evolutionary contingency is a big topic in philosophy of biology, and Bradbury has a great short story on this type of contingency.
Ray Bradbury is an interesting author—one who has many short stories and regular books. One of my favorite stories from Bradbury is one called A Sound of Thunder which chronicled a time machine company who let people go back in time to hunt any animal they’d like—if you want to take down the ancestor of a whale before it became aquatic, just name the place and they will send you there. They were told to only stay on the path laid out by the time machine company—animals they could shoot were marked with red paint, presumably those animals would have died anyway so killing them would not change any outcomes. The text from Bradbury is worth quoting in full, as it wonderfully captures the thought of evolutionary contingency:
He indicated a metal path that struck off into green wilderness, over streaming swamp, among giant ferns and palms. “And that,” he said, “is the Path, laid by Time Safari for your use, It floats six inches above the earth. Doesn’t touch so much as one grass blade, flower, or tree. It’s an anti-gravity metal. Its purpose is to keep you from touching this world of the past in any way. Stay on the Path. Don’t go off it. I repeat. Don’t go off. For any reason! If you fall off, there’s a penalty. And don’t shoot any animal we don’t okay.”
“Why?” asked Eckels.
They sat in the ancient wilderness. Far birds’ cries blew on a wind, and the smell of tar and an old salt sea, moist grasses, and flowers the color of blood.
“We don’t want to change the Future. We don’t belong here in the Past. The government doesn’t like us here. We have to pay big graft to keep our franchise. A Time Machine is finicky business. Not knowing it, we might kill an important animal, a small bird, a roach, a flower even, thus destroying an important link in a growing species.”
“That’s not clear,” said Eckels.
“All right,” Travis continued, “say we accidentally kill one mouse here. That means all the future families of this one particular mouse are destroyed, right?”
“Right”
“And all the families of the families of the families of that one mouse! With a stamp of your foot, you annihilate first one, then a dozen, then a thousand, a million, a billion possible mice!”
“So they’re dead,” said Eckels. “So what?”
“So what?” Travis snorted quietly. “Well, what about the foxes that’ll need those mice to survive? For want of ten mice, a fox dies. For want of ten foxes a lion starves. For want of a lion, all manner of insects, vultures, infinite billions of life forms are thrown into chaos and destruction. Eventually it all boils down to this: fifty-nine million years later, a caveman, one of a dozen on the entire world, goes hunting wild boar or saber-toothed tiger for food. But you, friend, have stepped on all the tigers in that region. By stepping on one single mouse. So the caveman starves. And the caveman, please note, is not just any expendable man, no! He is an entire future nation. From his loins would have sprung ten sons. From their loins one hundred sons, and thus onward to a civilization. Destroy this one man, and you destroy a race, a people, an entire history of life. It is comparable to slaying some of Adam’s grandchildren. The stomp of your foot, on one mouse, could start an earthquake, the effects of which could shake our earth and destinies down through Time, to their very foundations. With the death of that one caveman, a billion others yet unborn are throttled in the womb. Perhaps Rome never rises on its seven hills. Perhaps Europe is forever a dark forest, and only Asia waxes healthy and teeming. Step on a mouse and you crush the Pyramids. Step on a mouse and you leave your print, like a Grand Canyon, across Eternity. Queen Elizabeth might never be born, Washington might not cross the Delaware, there might never be a United States at all. So be careful. Stay on the Path. Never step off!”
“I see,” said Eckels. “Then it wouldn’t pay for us even to touch the grass?”
“Correct. Crushing certain plants could add up infinitesimally. A little error here would multiply in sixty million years, all out of proportion. Of course maybe our theory is wrong. Maybe Time can’t be changed by us. Or maybe it can be changed only in little subtle ways. A dead mouse here makes an insect imbalance there, a population disproportion later, a bad harvest further on, a depression, mass starvation, and finally, a change in social temperament in far-flung countries. Something much more subtle, like that. Perhaps only a soft breath, a whisper, a hair, pollen on the air, such a slight, slight change that unless you looked close you wouldn’t see it. Who knows? Who really can say he knows? We don’t know. We’re guessing. But until we do know for certain whether our messing around in Time can make a big roar or a little rustle in history, we’re being careful. This Machine, this Path, your clothing and bodies, were sterilized, as you know, before the journey. We wear these oxygen helmets so we can’t introduce our bacteria into an ancient atmosphere.”
This passage from Bradbury wonderfully illustrates evolutionary—historical—contingency. Things could have been different—this is the basis of the contingency argument. The universe does not repeat itself—if we were to replay the tape of life we would get a completely different outcome—Lane (2015) states maybe octopi would rule the earth? We could replay the tape of life, have it go exactly as it did to lead up to today, change ONE SEEMINGLY MINISCULE THING (say, stepping on a bug that did not die) which would then cascade throughout history leading to a change in the future. Evolution is full of passive trends, with no indication that—for example with body plans—that there is a drive to become more complex—it is passive (Gould, 1996: 207):
All the tests provide evidence for a passive trend and no drive to complexity. McShea found twenty-four cases of significant increases or decreases in comparing the range of modern descendants with an ancestor (out of a potential sample of ninety comparisons, or five groups of mammals, each with six variables measured in each of three ways; for the other comparison, average descendants did not differ significantly from ancestors). Interestingly, thirteen of these significant changes led to decreases in complexity, while only nine showed an increase. (The difference between thirteen and nine is not statistically significant, but I am wryly amused, given all traditional expectation in the other direction, that more comparisons show increasing rather than decreasing complexity.
Gould first put forth his contingency argument in Wonderful Life—any replay would be different then the next. Gould critiqued the increasing complexity claim, arguing that diversification is always accompanied by decimation—once a mass extinction (say, an asteroid impact) occurs, there will then be subsequent diversification after the decimation.
We have no idea why certain organisms persisted over others after periods of decimation—and ‘adaptation’ to environments cannot be the whole story. Out of all of Gould’s writing that I have read in my life, this passage is one of my favorites as it perfectly captures the problem at hand:
Wind the tape of life back to Burgess times, and let it play again. If Pikaia does not survive in the replay, we are wiped out of future history—all of us, from shark to robin to orangutan. And I don’t think that any handicapper, given Burgess evidence as known today, would have granted very favorable odds for the persistence of Pikaia.
And so, if you wish to ask the question of the ages—why do humans exist?—a major part of the answer, touching those aspects of the issue that science can treat at all, must be: because Pikaia survived the Burgess decimation. This response does not cite a single law of nature; it embodies no statement about predictable evolutionary pathways, no calculation of probabilities based on general rules of anatomy or ecology. The survival of Pikaia was a contingency of “just history.” I do not think that any “higher” answer can be given, and I cannot imagine that any resolution could be more fascinating. We are the offspring of history, and must establish our own paths in this most diverse and interesting of conceivable universes—one indifferent to our suffering, and therefore offering us maximal freedom to thrive, or to fail, in our own chosen way. (Gould, 1989: 323)
Contingency is about counterfactuals—what could have happened, what could have been, or what would have been had some certain condition changed, with everything before that occurring as usual. Bradbury’s A Sound of Thunder wonderfully illustrates the contingency of the evolutionary process—change one seemingly small, minuscule thing in the past and this could snowball and cascade to huge changes in the future—we may never have existed or we would have existed but have been radically different. If we could go back in time and, say, crush a butterfly and see the changes it would have made, we could say that the event that caused the future to change was the crushing of that butterfly—this could have, eventually, led to the non-existence of a certain group of people or a certain group of animals which would have radically changed the outcome of the world—both the natural and human world.
So, if we could replay life’s tape from the very beginning, I do believe that life as we know it would be different—for if we played it from the beginning, we could have a scenario as described by Bradbury—everything could go exactly the same with one small seemingly minuscule change snowballing into a world that we would barely recognize.
Just-so Stories: The Brain Size Increase
1600 words
The increase in brain size in our species over the last 3 million years has been the subject of numerous articles and books. Over that time period, brain size increased from our ancestor Lucy, all the way to today. Many stories are proposed to explain how and why it exactly happened. The explanation is the same ol’ one: Those with bigger heads, and therefore bigger brains had more children and passed on their “brain genes” to the next generation until all that was left was bigger-brained individuals of that species. But there is a problem here, just like with all just-so stories. How do we know that selection ‘acted’ on brain size and thusly “selected-for” the ‘smarter’ individual?
Christopher Badcock, an evolutionary psychologist, as an intro to EP published in 2001, where he has a very balanced take on EP—noting its pitfalls and where, in his opinion, EP is useful. (Most may know my views on this already, see here.) In any case, Badcock cites R.D. Martin (1996: 155) who writes:
… when the effects of confounding variables such as body size and socio-economic status are excluded, no correlation is found between IQ and brain size among modern humans.
Badcock (2001: 48) also quotes George Williams—author of Adaptation and Natural Selection (1966; the precursor to Dawkins’ The Selfish Gene) where he writes:
Despite the arguments that have been advanced, I cannot readily accept the idea that advanced mental capabilities have ever been directly favored by selection. There is no reason for believing that a genius has ever been likely to leave more children than a man of somewhat below average intelligence. It has been suggested that a tribe that produces an occasional genius for its leadership is more likely to prevail in competition with tribes that lack this intellectual resource. This may well be true in the sense that a group with highly intelligent leaders is likely to gain political domination over less gifted groups, but political domination need not result in genetic domination, as indicated by the failure of many a ruling class to maintain its members.
In Adaptation and Natural Selection, Williams was much more cautious than adaptationists today, stating that adaptationism should be used only in very special cases. Too bad that adaptationists today did not get the memo. But what gives? Doesn’t it make sense that the “more intelligent” human 2 mya would be more successful when it comes to fitness than the “less intelligent” (whatever these words mean in this context) individual? Would a pre-historic Bill Gates have the most children due to his “high IQ” as PumpkinPerson has claimed in the past? I doubt it.
In any case, the increase in brain size—and therefore increase in intellectual ability in humans—has been the last stand for evolutionary progressionists. “Look at the increase in brain size”, the progressionist says “over the past 3mya. Doesn’t it look like there is a trend toward bigger, higher-quality brains in humans as our skills increased?” While it may look like that on its face, in fact, the real story is much more complicated.
Deacon (1990a) notes many fallacies that those who invoke the brain size increase across evolutionary history make, including: the evolutionary progression fallacy; the bigger-is-smarter fallacy; and the numerology fallacy. The evolutionary progression fallacy is simple enough. Deacon (1990a: 194) writes:
In theories of brain evolution, the concept of evolutionary progress finds implicit expression in the analysis of brain-size differences and presumed grade shifts in allometric brain/body size trends, in theories of comparative intelligence, in claims about the relative proportions of presumed advanced vs. primitive brain areas, in estimates of neural complexity, including the multiplication and differentiation of brain areas, and in the assessment of other species with respect to humans, as the presumed most advanced exemplar. Most of these accounts in some way or other are tied to problems of interpreting the correlates of brain size. The task that follows is to dispose of fallacious progressivist notions hidden in these analyses without ignoring the questions otherwise begged by the many enigmatic correlations of brain size in vertebrate evolution.
Of course, when it comes to the bigger-is-smarter fallacy, it’s quite obviously not true that bigger IS always better when it comes to brain size, as elephants and whales have larger brains than humans (also see Skoyles, 1999). But what they do not have more of than humans is cortical neurons (see Herculano-Houzel, 2009). Decon (1990a: 201) describes the numerology fallacy:
Numerology fallacies are apparent correlations that turn out to be artifacts of numerical oversimplification. Numerology fallacies in science, like their mystical counterparts, are likely to be committed when meaning is ascribed to some statistic merely by virtue of its numeric similarity to some other statistic, without supportive evidence from the empirical system that is being described.
While Deacon (1990a: 232) concludes that:
The idea, that there have been progressive trends of brain evolution, that include changes in the relative proportions of different structures (i.e., enlarging more “advanced” areas with respect to more primitive areas) and increased differentiation, interconnection, and overall complexity of neural circuits, is largely an artifact of misunderstanding the complex internal correlates of brain size. … Numerous statistical problems, arising from the difficulty of analyzing a system with so many interdependent scaling relationships, have served to reinforce these misconceptions, and have fostered the tacit assumption that intelligence, brain complexity, and brain size bear a simple relationship to one another.
Deacon (1990b: 255) notes how brains weren’t directly selected for, but bigger bodies (bigger bodies means bigger brains), and this does not lean near the natural selection fallacy theory for trait selection since this view is of the organism, not its trait:
I will argue that it is this remarkable parallelism, and not some progressive selection for increasing intelligence, that is responsible for many pseudoprogressive trends in mammalian brain evolution. Larger whole animals were being selected—not just larger brains—but along with the correlated brain enlargement in each lineage a multitude of parallel secondary internal adaptations followed.
Deacon (1990b: 697-698) notes that the large brain-to-body size ratio in humans compared to other primates is an illusion “a surface manifestation of a complex allometric reorganization within the brain” and that the brain itself is unlikely to be the object of selection. The correlated reorganization of the human brain, to Deacon, is what makes humans unique; not our “oversized” brains for our body. While Deacon (1990c) states that “To a great extent the apparent “progress” of mammalian brain evolution vanishes when the effects of brain size and functional specialization are taken into account.” (See also Deacon, 1997: chapter 5.)
So is there really progress in brain evolution, which would, in effect, lend credence to the idea that evolution is progressive? No, there is no progress in brain evolution; so-called size increases throughout human history are an artifact; when we take brain size and functional specialization into account (functional specialization is the claim that different areas in the brain are specialized to carry out different functions; see Mahon and Cantlon, 2014). Our brains only seem like they’ve increased; when we get down to the functional details, we can see that it’s just an artifact.
Skoyles and Sagan (2002: 240) note that erectus, for example, could have survived with much smaller brains and that the brain of erectus did not arise for the need for survival:
So how well equipped was Homo erectus? To throw some figures at you (calculations shown in the notes), easily well enough. Of Nariokotome boy’s 673 cc of cortex, 164 cc would have been prefrontal cortex, roughly the same as half-brained people. Nariokotome boy did not need the mental competence required by cotemporary hunter-gatherers. … Compared to that of our distant ancestors, Upper Paleolithic technology is high tech. And the organizational skills used in hunts greatly improved 400,000 years ago to 20,000 years ago. These skills, in terms of our species, are recent, occurring by some estimates in less than the last 1 percent of our 2.5 million year existence as people. Before then, hunting skills would have required less brain power, as they were less mentally demanding. If you do not make detailed forward plans, then you do not need as much mental planning abilities as those who do. This suggests that the brains of Homo erectus did not arise for reasons of survival. For what they did, they could have gotten away with much smaller, Daniel Lyon-sized brains.
In any case—irrespective of the problems that Deacon shows for arguments for increasing brain size—how would we be able to use the theory of natural selection to show what was selected-for, brain size or another correlated trait? The progressionist may say that it doesn’t matter which is selected-for, the brain size is still increasing even if the correlated trait—the free-rider—is being selected-for.
But, too bad for the progressionist: If the correlated non-fitness-enhancing trait is being selected-for and not brain size directly, then the progressionist cannot logically state that brain size—and along with it intelligence (as the implication always is)—is being directly selected-for. Deacon throws a wrench into such theories of evolutionary progress in regard to human brain size. Though, looking at erectus, it’s not clear that he really “needed” such a big brain for survival—it seems like he could have gotten away with a much smaller brain. And there is no reason, as George Williams notes, to attempt to argue that “high intelligence” was selected-for in our evolutionary history.
And so, Gould’s Full House argument still stands—there is no progress in evolution; bacteria occupy life’s mode; humans are insignificant to the number of bacteria on the planet, “big brains”, or not.
Rampant Adaptationism
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Adaptationism is the main school of evolutionary change, through “natural selection” (NS). That is the only way for adaptations to appear, says the adaptationist: traits that were conducive to reproductive success in past environments were selected-for their contribution to fitness and therefore became fixated in the organism in question. That’s adaptationism in a nutshell. It’s also vacuous and tells us nothing interesting. In any case, the school of thought called adaptationism has been the subject of much criticism, most importantly, Gould and Lewontin (1972), Fodor (2008) and Fodor and Piatteli-Palmarini (2010). So, I would say that adaptationism becomes “rampant” when clearly cultural changes are conflated as having an evolutionary history and are still around today due to being adaptations.
Take Bret Weinstein’s recent conversation with Richard Dawkins:
Weinstein: “Understood through the perspective of German genes, vile as these behaviors were, they were completely comprehensible at the level of fitness. It was abhorrent and unacceptable—but understandable—that Germany should have viewed its Jewish population as a source of resources if you viewed Jews as non-people. And the belief structures that cause people to step onto the battlefields and fight were clearly comprehensible as adaptations of the lineages in question.”
Dawkins: “I think nationalism may be an even greater evil than religion. And I’m not sure that it’s actually helpful to speak of it in Darwinian terms.”
I find it funny that Weinstein is more of a Dawkins-ist than Dawkins himself is (in regard to his “selfish gene theory”, see Noble, 2011). In any case, what a ridiculous claim. “Guys, the Nazis were bad because of their genes and their genes made them view Jews as non-people and resources. Their behaviors were completely understandable at the level of fitness. But, Nazis bad!”
What a ridiculous claim. I like how Dawkins quickly shot the bullshit down. This is just-so storytelling on steroids. I wonder what “belief structures that cause people to step onto battlefields” are “adaptations of the lineages in question”? Do German belief structure adaptations different from any other groups? Can one prove that there are “belief structures” that are “adaptations to the lineages in question”? Or is Weinstein just telling just-so stories—stories with little evidence and that “fit” and “make sense” with the data we have (despicable Nazi behavior towards Jews after WWI and before and during WWII).
There is a larger problem with adaptationism, though: adaptationist confuse adaptiveness with adaptation (a trait can be adaptive without being an adaptation), they overlook nonadaptationist explanations, and adaptationist hypotheses are hard to falsify since a new story can be erected to explain the feature in question if one story gets disproved. That’s the dodginess of adaptationism.
An adaptationist may look at an organism, look at its traits, then construct a story as to why they have the traits they do. They will attempt to think of its evolutionary history by thinking of the environment it is currently in and what the traits in question that it has are useful for now. But there is a danger here. We can create many stories for just one so-called adaptation. How do we distinguish between which stories explain the fixation of the trait and which do not? We can’t: there is no way for us to know which of the causal stories explains the fixation of the trait.
Gould and Lewontin (1972) fault:
the adaptationist programme for its failure to distinguish current utility from reasons for origin (male tyrannosaurs may have used their diminutive front legs to titillate female partners, but this will not explain why they got so small); for its unwillingness to consider alternatives to adaptive stories; for its reliance upon plausibility alone as a criterion for accepting speculative tales; and for its failure to consider adequately such competing themes as random fixation of alleles, production of nonadaptive structures by developmental correlation with selected features (allometry, pleiotropy, material compensation, mechanically forced correlation), the separability of adaptation and selection, multiple adaptive peaks, and current utility as an epiphenomenon of nonadaptive structures.
[…]
One must not confuse the fact that a structure is used in some way (consider again the spandrels, ceiling spaces, and Aztec bodies) with the primary evolutionary reason for its existence and conformation.
Of course, though, adaptationists (e.g., evolutionary psychologists) do confuse structure for function. This is fallacious reasoning. That a trait is useful in a current environment is in no way evidence that it is an adaptation nor is it evidence that that’s why the trait evolved (e.g., a trait being useful and adaptive in a current environment).
But there is a problem with looking to the ecology of the organism in question and attempting to construct historical narratives about the evolution of the so-called adaptation. As Fodor and Piatteli-Palmarini (2010) note, “if evolutionary problems are individuated post hoc, it’s hardly surprising that phenotypes are so good at solving them.” So of course if an organism fails to secure a niche then that means that the niche was not for that organism.
That organisms are so “fit” to their environment, like a puzzle piece to its surrounding pieces, is supposed to prove that “traits are selected-for their contribution to fitness in a given ecology”, and this is what the theory of natural selection attempts to explain. Organisms fit their ecologies because its their ecologies that “design” their traits. So it is no wonder that organisms and their environments have such a tight relationship.
Take it from Fodor and Piatelli-Palmarini (2010: 137):
You don’t, after all, need an adaptationist account of evolution in order to explain the fact that phenotypes are so often appropriate to ecologies, since, first impressions to the contrary notwithstanding, there is no such fact. It is just a tautology (if it isn’t dead) a creature’s phenotype is appropriate for its survival in the ecology that it inhabits.
So since the terms “ecology” and “phenotype” are interdefined, is it any wonder why an organism’s phenotype has such a “great fit” with its ecology? I don’t think it is. Fodor and Piatteli-Palmarini (2010) note how:
it is interesting and false that creatures are well adapted to their environments; on the other hand it’s true but not interesting that creatures are well adapted to their ecologies. What, them, is the interesting truth about the fitness of phenotypes that we require adaptationism in order to explain? We’ve tried and tried, but we haven’t been able to think of one.
So the argument here could be:
P1) Niches are individuated post hoc by reference to the phenotypes that live in said niche.
P2) If the organisms weren’t there, the niche would not be there either.
C) Therefore there is no fitness of phenotypes to lifestyles that explain said adaptation.
Fodor and Piatteli-Palmarini put it bluntly about how the organism “fits” to its ecology: “although it’s very often cited in defence of Darwinism, the ‘exquisite fit’ of phenotypes to their niches is either true but tautological or irrelevant to questions about how phenotypes evolve. In either case, it provides no evidence for adaptationism.”
The million-dollar question is this, though: what would be evidence that a trait is an adaptation? Knowing what we now know about the so-called fit to the ecology, how can we say that a trait is an adaptation for problem X when niches are individuated post hoc? That right there is the folly of adaptationism, along with the fact that it is unfalsifiable and leads to just-so storytelling (Smith, 2016).
Such stories are “plausible”, but that is only because they are selected to be so. When such adaptationism becomes entrenched in thought, many traits are looked at as adaptations and then stories are constructed as to how and why the trait became fixated in the organism. But, just like EP which uses the theory of natural selection as its basis, so too does adaptationism fail. Nevermind the problem of the fitting of species to ecologies to render evolutionary problems post hoc; nevermind the problem that there is no identifying criteria for identifying adaptations; do mind the fact that there is no possible way for natural selection to do what it does: distinguish between coextensive traits.
In sum, adaptationism is a failed paradigm and we need to dispense with it. The logical problems with it are more than enough to disregard it. Sure, the fitness of a phenotype, say, the claws of a mole do make sense in the ecology it is in. But we only claim that the claws of a mole are adaptations after the fact, obviously. One may say “It’s obvious that the claws of a mole are adaptations, look at how it lives!” But this betrays a notion that Gould and Lewontin (1972) made: do not confuse structure with an evolutionary reason for its existence, which, unfortunately, many people do (most glaringly, evolutionary psychologists). Weinstein’s ridiculous claims about Nazi actions during WWII are a great example of how rampant adaptationism has become: we can explain any and all traits as an adaptation, we just need to be creative with the stories we tell. But just because we can create a story that “makes sense” and explains the observation does not mean that the story is a likely explanation for the trait’s existence.
Just-so Stories: MCPH1 and ASPM
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“Microcephalin, a gene regulating brain size, continues to evolved adaptively in humans” (Evans et al, 2005) “Adaptive evolution of ASPM, a major determinant of cerebral cortical size in humans” (Evans et al, 2004) are two papers from the same research team which purport to show that both MCPH1 and ASPM are “adaptive” and therefore were “selected-for” (see Fodor, 2008; Fodor and Piatteli-Palmarini, 2010 for discussion). That there was “Darwinian selection” which “operated on” the ASPM gene (Evans et al, 2004), that we identified it was selected, along with its functional effect is evidence that it was supposedly “selected-for.” Though, the combination of functional effect along with signs of (supposedly) positive selection do not license the claim that the gene was “selected-for.”
One of the investigators who participated in these studies was one Bruce Lahn, who stated in an interview that MCPH1 “is clearly favored by natural selection.” Evans et al (2005) show specifically that the variant supposedly under selection (MCPH1) showed lower frequencies in Africans and the highest in Europeans.
But, unfortunately for IQ-ists, neither of these two alleles are associated with IQ. Mekel-Boborov et al (2007: 601) write that their “overall findings suggest that intelligence, as measured by these IQ tests, was not detectably associated with the D-allele of either ASPM or Microcephalin.” Timpson et al (2007: 1036A) found “no meaningful associations with brain size and various cognitive measures, which indicates that contrary to previous speculations, ASPM and MCPH1 have not been selected for brain-related effects” in genotyped 9,000 genotyped children. Rushton, Vernon, and Bons (2007) write that “No evidence was found of a relation between the two candidate genes ASPM and MCPH1 and individual differences in head circumference, GMA or social intelligence.” Bates et al’s (2008) analysis shows no relationship between IQ and MCPH1-derived genes.
But, to bring up Fodor’s critique, if MCPH1 is coextensive with another gene, and both enhance fitness, then how can there be direct selection on the gene in question? There is no way for selection to distinguish between the two linked genes. Take Mekel-Bobrov et al (2005: 1722) who write:
The recent selective history of ASPM in humans thus continues the trend of positive selection that has operated at this locus for millions of years in the hominid lineage. Although the age of haplogroup D and its geographic distribution across Eurasia roughly coincide with two important events in the cultural evolution of Eurasia—namely, the emergence and spread of domestication from the Middle East ~10,000 years ago and the rapid increase im population associated with the development of cities and written language 5000 to 6000 years ago around the Middle East—the signifigance of this correlation is not clear.
Surely both of these genetic variants have a hand in the dawn of these civilizations and behaviors of our ancestors; they are correlated, right? Though, they only did draw that from the research studies they reported on—these types of wild speculation are in the papers referenced above. Lahn and his colleagues, though, are engaging in very wild speculation—if these variants are under positive selection, that is.
So it seems that this research and the conclusions drawn from it are ripe for a just-so story. We need to do a just-so story check. Now let’s consult Smith’s (2016: 277-278) seven just-so story triggers:
1) proposing a theory-driven rather than a problem-driven explanation, 2) presenting an explanation for a change without providing a contrast for that change, 3) overlooking the limitations of evidence for distinguishing between alternative explanations (underdetermination), 4) assuming that current utility is the same as historical role, 5) misusing reverse engineering, 6) repurposing just-so stories as hypotheses rather than explanations, and 7) attempting to explain unique events that lack comparative data.
For example, take (1): a theory-driven explanation leads to a just-so story, as Shapiro (2002: 603) notes, “The theory-driven scholar commits to a sufficient account of a phenomenon, developing a “just so” story that might seem convincing to partisans of her theoretical priors. Others will see no more reason to believe it than a host of other “just so” stories that might have been developed, vindicating different theoretical priors.” That these two genes were “selected-for” means that, for Evans et al, it is a theory-driven explanation and therefore falls prey to the just-so story criticism.
Rasmus Nielsen (2009) has a paper on the thirty years of adaptationism after Gould and Lewontin’s (1972) Spandrels paper. In it, he critiques so-called examples of two genes being supposedly selected-for: a lactase gene, and MCPH1 and ASPM. Nielsen (2009) writes of MCPH1 and ASPM:
Deleterious mutations in ASPM and microcephalin may lead to reduced brain size, presumably because these genes are cell‐cycle regulators and very fast cell division is required for normal development of the fetal brain. Mutations in many different genes might cause microcephaly, but changes in these genes may not have been the underlying molecular cause for the increased brain size occurring during the evolution of man.
In any case, Currat et al (2006: 176a) show that “the high haplotype frequency, high levels of homozygosity, and spatial patterns observed by Mekel-Bobrov et al. (1) and Evans et al. (2) can be generated by demographic models of human history involving a founder effect out-of-Africa and a subsequent demographic or spatial population expansion, a very plausible scenario (5). Thus, there is insufficient evidence for ongoing selection acting on ASPM and microcephalin within humans.” McGowen et al (2011) show that there is “no evidence to support an association between MCPH1 evolution and the evolution of brain size in highly encephalized mammalian species. Our finding of significant positive selection in MCPH1 may be linked to other functions of the gene.”
Lastly, Richardson (2011: 429) writes that:
The force of acceptance of a theoretical framework for approaching the genetics of human intellectual differences may be assessed by the ease with which it is accepted despite the lack of original empirical studies – and ample contradictory evidence. In fact, there was no evidence of an association between the alleles and either IQ or brain size. Based on what was known about the actual role of the microcephaly gene loci in brain development in 2005, it was not appropriate to describe ASPM and microcephalin as genes controlling human brain size, or even as ‘brain genes’. The genes are not localized in expression or function to the brain, nor specifically to brain development, but are ubiquitous throughout the body. Their principal known function is in mitosis (cell division). The hypothesized reason that problems with the ASPM and microcephalin genes may lead to small brains is that early brain growth is contingent on rapid cell division of the neural stem cells; if this process is disrupted or asymmetric in some way, the brain will never grow to full size (Kouprina et al, 2004, p. 659; Ponting and Jackson, 2005, p. 246)
Now that we have a better picture of both of these alleles and what they are proposed to do, let’s now turn to Lahn’s comments on his studies. Lahn, of course, commented on “lactase” and “skin color” genes in defense of his assertion that such genes like ASPM and MCPH1 are linked to “intelligence” and thusly were selected-for just that purpose. However, as Nielsen (2009) shows, that a gene has a functional effect and shows signs of selection does not license the claim that the gene in question was selected-for. Therefore, Lahn and colleagues engaged in fallacious reasoning; they did not show that such genes were “selected-for”, while even studies done by some prominent hereditarians did not show that such genes were associated with IQ.
Like what we now know about the FOXP2 gene and how there is no evidence for recent positive or balancing selection (Atkinson et al, 2018), we can now say the same for such other evolutionary just-so stories that try to give an adaptive tinge to a trait. We cannot confuse selection and function as evidence for adaptation. Such just-so stories, like the one described above along with others on this blog, can be told about any trait or gene and explain why it was selected and stabilized in the organism in question. But historical narratives may be unfalsifiable. As Sterelny and Griffiths write in their book Sex and Death:
Whenever a particular adaptive story is discredited, the adaptationist makes up a new story, or just promises to look for one. The possibility that the trait is not an adaptation is never considered.
The Modern Synthesis vs the Extended Evolutionary Synthesis
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The Modern Synthesis (MS) has entrenched evolutionary thought since its inception in the mid-1950s. The MS is the integreation of Darwinian natural selection and Mendelian genetics. Key assumptions include “(i) evolutionarily significant phenotypic variation arises from genetic mutations that occur at a low rate independently of the strength and direction of natural selection; (ii) most favourable mutations have small phenotypic effects, which results in gradual phenotypic change; (iii) inheritance is genetic; (iv) natural selection is the sole explanation for adaptation; and (v) macro-evolution is the result of accumulation of differences that arise through micro-evolutionary processes” (Laland et al, 2015).
Laland et al (2015) even have a helpful table on core assumptions of both the MS and Extended Evolutionary Synthesis (EES). The MS assumptions are on the left while the EES assumptions are on the right.
Darwinian cheerleaders, such as Jerry Coyne and Richard Dawkins, would claim that neo-Darwinisim can—and already does—account for the assumptions of the EES. However, it is clear that that claim is false. At its core, the MS is a gene-centered perspective whereas the EES is an organism-centered perspective.
To the followers of the MS, evolution occurs through random mutations and change in allele frequencies which then get selected for by natural selection since they lead to an increase in fitness in that organism, and so, that trait that the genes ’cause’ then carry on to the next generation due to its contribution to fitness in that organism. Drift, mutation and gene flow also account for changes in genetic frequencies, but selection is the strongest of these modes of evolution to the Darwinian. The debate about the MS and the EES comes down to gene-selectionism vs developmental systems theory.
On the other hand, the EES is an organism-centered perspective. Adherents to the EES state that the organism is inseparable from its environment. Jarvilehto (1998) describes this well:
The theory of the organism-environment system (Jairvilehto, 1994, 1995) starts with the proposition that in any functional sense organism and environment are inseparable and form only one unitary system. The organism cannot exist without the environment and the environment has descriptive properties only if it is connected to the organism.
At its core, the EES makes evolution about the organism—its developmental system—and relegates genes, not as active causes of traits and behaviors, but as passive causes, being used by and for the system as needed (Noble, 2011; Richardson, 2017).
One can see that the core assumptions of the MS are very much like what Dawkins describes in his book The Selfish Gene (Dawkins, 1976). In the book, Dawkins claimed that we are what amounts to “gene machines”—that is, just vehicles for the riders, the genes. So, for example, since we are just gene machines, and if genes are literally selfish “things”, then all of our actions and behaviors can be reduced to the fact that our genes “want” to survive. But the “selfish gene” theory “is not even capable of direct empirical falsification” (Noble, 2011) because Richard Dawkins emphatically stated in The Extended Phenotype (Dawkins, 1982: 1) that “I doubt that there is any experiment that could prove my claim” (quoted in Noble, 2011).
Noble (2011) goes on to discuss Dawkins’ view that on genes:
Now they swarm in huge colonies, safe inside gigantic lumbering robots, sealed off from the outside world, communicating with it by tortuous indirect routes, manipulating it by remote control. They are in you and me; they created us, body and mind; and their preservation is the ultimate rationale for our existence. (1976, 20)
Noble then switches the analogy: Noble likens genes, not as having a “selfish” attribute, but to that of being “prisoners”, stuck in the body with no way of escape. Noble then says that, since there is no experiment to distinguish between the two views (which Dawkins admitted). Noble then concludes that, instead of being “selfish”, the physiological sciences look at genes as “cooperative”, since they need to “cooperate” with the environment, other genes, gene networks etc which comprise the whole organism.
In his 2018 book Agents and Goals in Evolution Samir Okasha distinguishes between type I and type II agential thinking. “In type 1 [agential thinking], the agent with the goal is an evolved entity, typically an individual organism; in type 2, the agent is ‘mother nature’, a personification of natural selection” (Okasha, 2018: 23). An example of type I agential thinking is Dawkins’ selfish genes, while type II is the personification that one imputes onto natural selection—which Okasha states that this type of thinking “Darwin was himself first to employ” (Okasha, 2018: 36) it.
Okasha states that each gene’s ultimate goal is to outcompete other genes—for that gene in question to increase its frequency in the organism. They also can have intermediate goals which is to maximize fitness. Okasha gives three rationales on what makes something “an agent”: (1) goal-directedness; (2) behavioral flexibility; and (3) adaptedness. So the “selfish” element “constitutes the strongest argument for agential thinking” of the genes (Okasha, 2018: 73). However, as Denis Noble has tirelessly pointed out, genes (DNA sequences) are inert molecules (and are one part of the developing system) and so do not show behavioral flexibility or goal-directedness. Genes can (along with other parts of the system working in concert with them) exert adaptive effects on the phenotype, though when genes (and traits) are coextensive, selection cannot distinguish between the fitness-enhancing trait and the free-riding trait so it only makes logical sense to claim that organisms are selected, not any individual traits (Fodor and Piatteli-Palmarini, 2010a, 2010b).
It is because of this, that the Neo-Darwinian gene-centric paradigm has failed, and is the reason why we need a new evolutionary synthesis. Some only wish to tweak the MS a bit in order to allow what the MS does not incorporate in it, but others want to overhaul the entire thing and extend it.
Here is the main reason why the MS fails: there is absolutely no reason to privilege any level of the system above any other! Causation is multi-level and constantly interacting. There is no a priori justification for privileging any developmental variable over any other (Noble, 2012, 2017). Both downward and upward causation exists in biological systems (which means that molecules depend on organismal context). The organism also able to control stochasticity—which is “used to … generate novelty” (Noble and Noble, 2018). Lastly, there is the creation of novelty at new levels of selection, like with how the organism is an active participant in the construction of the environment.
Now, what does the EES bring that is different from the MS? A whole bunch. Most importantly, it makes a slew of novel predictions. Laland et al (2016) write:
For example, the EES predicts that stress-induced phenotypic variation can initiate adaptive divergence in morphology, physiology and behaviour because of the ability of developmental mechanisms to accommodate new environments (consistent with predictions 1–3 and 7 in table 3). This is supported by research on colonizing populations of house finches [68], water fleas [132] and sticklebacks [55,133] and, from a more macro-evolutionary perspective, by studies of the vertebrate limb [57]. The predictions in table 3 are a small subset of those that characterize the EES, but suffice to illustrate its novelty, can be tested empirically, and should encourage deriving and testing further predictions.
[Table 3]
There are other ways to verify EES predictions, and they’re simple and can be done in the lab. In his book Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics, philosopher of biology Jan Baedke notes that studies of epigenetic processes which are induced in the lab and those that are observed in nature are similar in that they share the same methodological framework. So we can use lab-induced epigenetic processes to ask evolutionary questions and get evolutionary answers in an epigenetic framework. There are two problems, though. One, that we don’t know whether experimental and natural epigenetic inducements will match up; and two we don’t know whether or not these epigenetic explanations that focus on proximate causes and not ultimate causes can address evolutionary explananda. Baedke (2018: 89) writes:
The first has been addressed by showing that studies of epigenetic processes that are experimentally induced in the lab (in molecular epigenetics) and those observed in natural populations in the field (in ecological or evolutionary epigenetics) are not that different after all. They share a similar methodological framework, one that allows them to pose heuristically fruitful research questions and to build reciprocal transparent models. The second issue becomes far less fundamental if one understands the predominant reading of Mayr’s classical proximate-ultimate distinction as offering a simplifying picture of what (and how) developmental explanations actually explain. Once the nature of developmental dependencies has been revealed, the appropriateness of developmentally oriented approaches, such as epigenetics, in evolutionary biology is secured.
Further arguments for epigenetics from an evolutionary approach can be found in Richardson’s (2017) Genes, Brains, and Human Potential (chapter 4 and 5) and Jablonka and Lamb’s (2005) Evolution in Four Dimensions. More than genes alone are passed on and inherited, and this throws a wrench into the MS.
Some may fault DST for not offering anything comparable to Darwinisim, as Dupre (2003: 37) notes:
Critics of DST complain that it fails to offer any positive programme that has achievements comparable to more orthodox neo-Darwinism, and so far this complaint is probably justified.
But this is irrelevant. For if we look at DST as just a part of the whole EES programme, then it is the EES that needs to—and does—“offer a positive programme that has achievements comparable to more orthodox neo-Darwinism” (Dupre, 2003: 37). And that is exactly what the EES does: it makes novel predictions; it explains what needs to be explained better than the MS; and the MS has shown to be incoherent (that is, there cannot be selection on only one level; there can only be selection on the organism). That the main tool of the MS (natural selection) has been shown by Fodor to be vacuous and non-mechanistic is yet another strike against it.
Since DST is a main part of the EES, and DST is “a wholeheartedly epigenetic approach to development, inheritance and evolution” (Griffiths, 2015) and the EES incorporates epigenetic theories, then the EES will live or die on whether or not its evolutionary epigenetic theories are confirmed. And with the recent slew of books and articles that attest to the fact that there is a huge component to evolutionary epigenetics (e.g., Baedke, 2018; Bonduriansky and Day, 2018; Meloni, 2019), it is most definitely worth seeing what we can find in regard to evolutionary epigenetics studies, since epigenetic changes induced in the lab and those that are observed in natural populations in nature are not that different. This can then confirm or deconfirm major hypotheses of the EES—of which there are many. It is time for Lamarck to make his return.
It is clear that the MS is lacking, as many authors have pointed out. To understand evolutionary history and why organisms have the traits they do, we need much more than the natural selection-dominated neo-Darwinian Modern Synthesis. We need a new synthesis (which has been formulated for the past 15-20 years) and only through this new synthesis can we understand the hows and whys. The MS was good when we didn’t know any better, but the reductionism it assumes is untenable; there cannot be any direct selection on any level (i.e., the gene) so it is a nonsensical programme. Genes are not directly selected, nor are traits that enhance fitness. Whole organisms and their developmental systems are selected and propagate into future generations.
The EES (and DST along with it) hold right to the causal parity thesis—“that genes/DNA play an important role in development, but so do other variables, so there is no reason to privilege genes/DNA above other developmental variables.” This causal parity between all tools of development is telling: what is selected is not just one level of the system, as genetic reductionists (neo-Darwinists) would like to believe; it occurs on the whole organism and what it interacts with (the environment); environments are inherited too. Once we purge the falsities that were forced upon us by the MS in regard to organisms and their relationship with the environment and the MS’s assumptions about evolution as a whole, we can then truly understand how and why organisms evolve the phenotypes they do; we cannot truly understand the evolution of organisms and their phenotypes with genetic reductionist thinking with sloppy logic. So who wins? The MS does not, since it has causation in biology wrong. This only leaves us with the EES as the superior theory, predictor, and explainer.
Book Review: “Lamarck’s Revenge”
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I recently bought Lamarck’s Revenge by paleobiologist Peter Ward (2018) because I went on a trip and needed something to read on the flight. I just finished the book the other day and I thought that I would give a review and also discuss Coyne’s review of the book since I know he is so uptight about epigenetic theories, like that of Denis Noble and Jablonka and Lamb. In Lamarck’s Revenge, Ward (2018) purports to show that Lamarck was right all along and that the advent of the burgeoning field is “Lamarck’s revenge” for those who—in the current day—make fun of his theories in intro biology classes. (When I took Bio 101, the professor made it a point to bring up Lamarck and giraffe necks as a “Look at this wrong theory”, nevermind the fact that Darwin was wrong too.) I will go chapter-by-chapter, give a brief synopsis of each, and then discuss Coyne’s review.
In the introduction, Ward discusses some of the problems with Darwinian thought and current biological understanding. The current neo-Darwinian Modern Synthesis states that what occurs in the lifetime of the organism cannot be passed down to further generations—that any ‘marks’ on the genome are then erased. However, recent research has shown that this is not the case. Numerous studies on plants and “simpler” organisms refute the notion, though for more “complex” organisms it has yet to be proved. However, that this discussion is even occurring is proof that we are heading in the right direction in regard to a new synthesis. In fact, Jablonka and Lamb (2005) showed in their book Evolution in Four Dimensions, that epigenetic mechanisms can and do produce rapid speciation—too quick for “normal” Darwinian evolution.
Ward (2018: 3-4) writes:
There are good times and bad times on earth, and it is proposed here that dichotomy has fueled a coupling of times when evolution has been mainly through Darwinian evolution and others when Lamarckian evolution has been dominant. Darwinian in good times, Lamarckian in bad, when bad can be defined as those times when our environments turn topsy-turvy, and do so quickly. When an asteroid hits the planet. When giant volcanic episodes create stagnant oceans. When a parent becomes a sexual predator. When our industrial output warms the world. When there are six billion humans and counting.
These examples are good—save the one about when a parent becomes a sexual predator (but if we accept the thesis that what we do and what happens to us can leave marks on our DNA that don’t change it but are passed on then it is OK)—and they all point to one thing: when the environment becomes ultra-chaotic. When such changes occur in the environment, that organism needs a physiology that is able to change on-demand to survive (see Richardson, 2017).
Ward (2018: 8) then describes Lamarck’s three-step process:
First, an animal experienced a radical change of the environment aroujnd it. Second, the initial response to the environmental change was some new kind of behavior by that of the animal (or whole species). Third, the behavioral change was followed by morphological change in subsequent generations.
Ward then discusses others before Darwin—Darwin’s grandfather Erasmus, for instance—who had theories of evolution before Darwin. In any case, we went from a world in which a God created all to a world where everything we see was created by natural processes.
Then in Chapter 2, Ward discusses Lamarck and Darwin and each of their theories in turn. (Note that Darwin did have Lamarckian views too.) Ward discusses the intellectual dual between Lamarck and Georges Cuvier, the father of the field of comparative anatomy—he studied mass extinctions. At Lamarck’s funeral, Cuvier spoke bad about Lamarck and buried his theories. (See Cuvier’s (1836) Elegy of Lamarck.) These types of arguments between academics have been going on for hundreds of years—and they will not stop any time soon.
In Chapter 3 Ward discusses Darwin’s ideas all the way to the Modern Synthesis, discussing how Darwin formulated his theory of natural selection, the purported “mechanism of evolution.” Ward discusses how Darwin at first rejected Lamarck’s ideas but then integrated them into future editions of On the Origin. We can think of this scenario: Imagine any environment and organisms in it. The environment rapidly shifts to where it is unrecognizable. The organisms in that environment then need to either change their behavior (and reproduce) or die. Now, if there were no way for organisms to change, say, their physiology (since physiology is dependent on what is occurring in the outside environment), then the species would die and there would be no evolution. However, the advent of evolved physiologies changed that. Morphologic and physiologic plasticity can and does help organisms survive in new environments—environments that are “new” to the parental organism—and this is a form of Lamarckism (“heritable epigenetics” as Ward calls it).
Chapter 4 discusses epigenetics and a newer synthesis. In the beginning of the chapter, Ward discusses a study he was a part of (Vandepas, et al, 2016). (Read Ward’s Nautilus article here.)
They studied two (so-called) different species of nautilus—one, nautilus pampilus, widespread across the Pacific and Indian Oceans and two, Nautilus stenomphalus which is only found at the Great Barrier Reef. Pompilus has a hole in the middle of its shell, whereas stenomphalus has a plug in the middle. Both of these (so-called) species have different kinds of anatomy—Pompilus has a hood covered with bumps of flesh whereas stenomphalus‘ hood is filled with projections of moss-like twig structures. So over a thirty-day period, they captured thirty nautiluses and snipped a piece of their tentacles and sequences the DNA found in it. They found that the DNA of these two morphologically different animals was the same. Thus, although the two are said to be different species based on their morphology, genetically they are the same species which leads Ward (2018: 52) to claim “that perhaps there are fewer, not more, species on Earth than science has defined.” Ward (2018: 53) cites a recent example—the fact that the Columbian and North American wooly mammoths “were genetically the same but the two had phenotypes determined by environment” (see Enk et al, 2011).
Now take Ward’s (2018: 58) definition of “heritable epigenetics”:
In heritable epigenetics, we pass on the same genome, but one marked (mark is the formal term for the place that a methyl molecule attaches to one nucleotide, a rung in the ladder of DNA) in such a way that the new organism soon has its own DNA swarmed by these new (and usually unwelcome) additions riding on the chromosomes. The genotype is not changed, but the genes carrying the new, sucker-like methyl molecules change the workings of the organism to something new, such as the production (or lack thereof) of chemicals necessary for our good health, or for how some part of the body is produced.
Chapter 5 discusses different environments in the context of evolutionary history. Environmental catastrophes that lead to the decimation of most life on the planet are the subject—something that Gould wrote about in his career (his concept of contingency in the evolutionary process). Now, going back to Lamarck’s dictum (first an environmental change, second a change in behavior, and third a change in phenotype), we can see that these kinds of processes were indeed imperative in the evolution of life on earth. Take the asteroid impact (K-Pg extinction; Cretaceous-Paleogene) that killed off the dinosaurs and threw tons of soot into the air, blocking out the sun making it effectively night (Schulte et al, 2010). All organisms that survived needed to eat. If the organism only ate in the day time, it would then need to eat at night or die. That right there is a radical environmental change (step 1) and then a change in behavior (step 2) which would eventually lead to step 3.
In Chapter 6, Ward discusses epigenetics and the origins of life. The main subject of the chapter is lateral gene transfer—the transmission of different DNA between genomes. Hundreds or thousands of new genes can be inserted into an organism and effectively change the morphology, it is a Lamarckian mechanism. Ward posits that there were many kinds of “genetic codes” and “metabolisms” throughout earth’s history, even organisms that were “alive” but were not capable of reproducing and so they were “one-offs.” Ward even describes Margulis’ (1967) theory of endosymbiosis as “a Lamarckian event“, which even Margulis accepts. Thus, the evolution of organisms is possible through lateral gene transfer and is another Lamarckian mechanism.
Chapter 7 discusses epigenetics and the Cambrian explosion. Ward cites a Creationist who claims that there has not been enough time since the 500 million year explosion to explain the diversity of body plans since then. Stephen Jay Gould wrote a whole book on this—Wonderful Life. It is true that Darwinian theory cannot explain the diversity of body plans, nor even the diversity of species and their traits (Fodor and Piatelli-Palmarini, 2010), but this does not mean that Creationism is true. If we are discussing the diversification of organismal life after mass extinctions, then Darwinian evolution cannot have possibly played a role in the survival of species—organisms with adaptive physiologies would have had a better chance of surviving in these new, chaotic environments.
It is posited here that four different epigenetic mechanisms presumably contributed to the great increase in both the kinds of species and the kinds of morphologies that distinguished them that together produced the Cambrian explosion as we currently know it: the first, now familiar, methylation; second, small RNA silencing; third, changes in the histones, the scaffolding that dictates the overall shape of a DNA molecule; and, finally, lateral gene transfer, which has recently been shown to work in animals, not just microbes. (Ward, 2018: 113)
Ginsburg and Jablonka (2010) state that “[associative] learning-based diversification was
accompanied by neurohormonal stress, which led to an ongoing destabilization and re-patterning of the epigenome, which, in turn, enabled further morphological, physiological, and behavioral diversification.” So associative learning, according to Ginsburg and Jablonka, was the driver of the Cambrian explosion. Ward (2018: 115) writes:
[The paper by Ginsburg and Jablonka] says that changes of behavior by both animal predators and animal prey began as an “arms race” in not just morphology but behavior. Learning how to hunt or flee; detecting food and mats and habitats at a distance from chemical senses of smell or vision, or from deciphering vibrations coming through water. Yet none of that would matter if the new behaviors and abilities were not passed on. As more animal body plans and the species they were composed of appeared, ecological communities changed radically and quickly. The epigenetic systems in snimals were, according to the authors, “destabilized,” andin reordering them it allowed new kinds of morphology, physiology, and again behavior, ans amid this was the ever-greater use of powerful hormone systems. Seeinf an approaching predator was not enough. The recognition of imminent danger would only save an animal’s life if its whole body was alerted and put on a “war footing” by the flooding of the creature with stress hormones. Poweful enactors of action. Over time, these systems were made heritable and, according to the authors, the novel evolution of fight or flight chemicals would have greatly enhanced survivability and success of early animals “enabled animals to exploit new niches, promoted new types of relations and arms races, and led to adaptive repsonses that became fixed through genetics.”
That, and vision. Brains, behavior, sense organs and hormones are tied to the nervous system to the digestive system. No single adaption led to animal success. It was the integration of these disparate systems into a whole that fostered survivability, and fostered the rapid evolution of new kinds of animals during the evolutionary fecund Cambrian explosion.
So, ever-changing environments are how physiological systems evolved (see Richardson, 2017: Chapters 4 and 5). Therefore, if the environment were static, then physiologies would not have evolved. Ever-changing environments were imperative to the evolution of life on earth. For if this were not the case, organisms with complex physiologies (note that a physiological system is literally a whole complex of cells) would never have evolved and we would not be here.
In chapter 8 Ward discusses epigenetic processes before and after mass extinctions. He states that, to mass extinction researchers, there are 3 ways in which mass extinction have occurred: (1) asteroid or comet impact; (2) greenhouse mass extinction events; and (3) glaciation extinction events. So these mass extinctions caused the emergence of body plans and new species—brought on by epigenetic mechanisms.
Chapter 9 discusses good and bad times in human history—and the epigenetic changes that may have occurred. Ward (2018: 149) discusses the Toba eruption and that “some small group of survivors underwent a behavioral change that became heritable, producing cultural change that is difficult to overstate.” Environmental change leads to behavioral change which eventually leads to change in morphology, as Lamarck said, and mass extinction events are the perfect way to show what Lamarck was saying.
In chapter 10 Ward discusses epigenetics and violence, the star of the chapter being MAOA. Take this example from Ward (2018: 167-168):
Causing violent death or escaping violent death or simply being subjected to intense violence causes significant flooding of the body with a whole pharmacological medicine chest of proteins, and in so doing changes the chemical state of virtually every cell. The produces epigenetic change(s) that can, depending on the individual, create a newly heritable state that is passed on to the offspring. The epigenetic change caused by the fight-or-flight response may cause progeny to be more susceptible to causing violence.
Ward then discsses MAOA (pg 168-170), though read my thoughts on the matter. (He discusses the role of epigenetics in the “turning on” of the gene. Child abuse has been shown to cause epigenetic changes in the brain (Zannas et al, 2015). (It’s notable that Ward—rightly—in this chapter dispenses with the nature vs. nurture argument.)
In Chapter 11, Ward discusses food and famine changing our DNA. He cites the most popular example, that of the studies done on survivors who bore children during or after the famine. (I have discussed this at length.) In September of 1944, the Dutch ordered a nation-wide railroad strike. The Germans then restricted food and medical access to the country causing the deaths of some 20,000 people and harming millions more. So those who were in the womb during the famine had higher rates of disorders such as obesity, anorexia, obesity, and cardiovascular incidences.
However, one study showed that if one’s father had little access to food during the slow growth period, then cardiovascular disease mortality was low. But diabetes mortality was high when the paternal grandfather was exposed to excess food. Further, when SES factors were controlled for, the difference in lifespan was 32 years, which was dependent on whether or not the grandfather was exposed to an overabundance of food or lack of abundance of food just before puberty.
Nutrition can alter the epigenome (Zhang and Kutateladze, 2018), since it can alter the epigenome and the epigenome is heritable, then these changes can be passed on to future generations too.
Ward then discusses the microbiome and epigenetics (read my article for a primer on the microbiome, what it does, and racial differences in it). The microbiome has been called “the second genome” (Grice and Segre, 2012), and so, any changes to the “second genome” can also be passed down to subsequent generations.
In Chapter 12, Ward discusses epigenetics and pandemics. Seeing people die from horrible diseases of course has horrible effects on people. Yes, there were evolutionary implications from these pandemics in that the gene pool was decreased—but what of the effects on the survivors? Methylation impacts behavior and behavior impacts methylation (Lerner and Overton, 2017), and so, differing behaviors after such atrocities can be tagged on the epigenome.
Ward then takes the discussion on pandemics and death and shifts to religion. Imagine seeing your children die, would you not want to believe that there was a better place for them after death to—somewhat—quell your sorrow over their loss? Of course, having an epiphany about something (anything, not just religon) can change how you view life. Ward also discusses a study where atheists had different brain regions activated even while no stimulation was presented. (I don’t like brain imaging studies, see William Uttal’s books and papers.) Ward also discusses the VMAT2 gene, which “controls” mood through the production of the VMAT protein, elevating hormones such as dopamine and serotonin (similar to taking numerous illegal drugs).
Then in Chapter 13 he discusses chemicals and toxins and how they relate to epigenetic processes. These kinds of chemicals and toxins are linked with changes in DNA methylation, miroRNAs, and histone modifications (Hou et al, 2012). (Also see Tiffon, 2018 for more on chemicals and how they affect the epigenome.)
Finally, in Chapter 14 Ward discusses the future of evolution in a world with CRISPR-CAS9. He discusses many ways in which the technology can be useful to us. He discusses one study in which Chinese scientists knocked out the myostatin gene in 65 dog embryos. Twenty-seven of the dogs were born and only two—a male and a female—had both copies of the myostatin gene disrupted. This is just like when researchers made “double-muscle” cattle. See my article ‘Double-Muscled’ Humans?
He then discusses the possibility of “supersoldiers” and if we can engineer humans to be emotionless killing machines. Imagine being able to engineer humans that had no sympathy, no empathy, that looked just like you and I. CRISPR is a tool that uses epigenetic processes and, thus, we can say that CRISPR is a man-made Lamarckian mechanism of genetic change (mimicking lateral gene transfer).
Now, let’s quickly discuss Coyne’s review before I give my thoughts on the book. He criticizes Ward’s article linked above (Coyne admits he did not read the book), stating that his claim that the two nautiluses discussed above being the same species with the same genome and epigenetic forces leading to differences in morphology (phenotype). Take Coyne’s critique of Vandepas, et al, 2016—that they only sequenced two mitochondrial genes. Combosch et al (2017; of which Ward was a coauthor) write (my emphasis):
Moreover, previous molecular phylogenetic studies indicate major problems with the conchiological species boundaries and concluded that Nautilus represents three geographically distinct clades with poorly circumscribed species (Bonacum et al, 2011; Ward et al, 2016). This is been reiterated in a more recent study (Vandepas et al, 2016), which concluded that N. pompilius is a morphologically variable species and most other species may not be valid. However, these studies were predominantly or exclusively based on mitochondrial DNA (mtDNA), an informative but often misleading marker for phylogenetic inference (e.g., Stöger & Schrödl 2013) which cannot reliably confirm and/or resolve the genetic composition of putative hybrid specimens (Wray et al, 1995).
Looks like Coyne did not look hard enough for more studies on the matter. In any case, it’s not just Ward that makes this argument—many other researchers do (see e.g., Tajika et al, 2018). So, if there is no genetic difference between these two (so-called) species, and they have morphological differences, then the possibility that seems likely is that the differences in morphology are environmentally-driven.
Lastly, Coyne was critical of Ward’s thoughts on the heritability of histone modification, DNA methylation, etc. It seems that Coyne has not read the work of philosopher Jan Baedke (see his Google Scholar page), specifically his book Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics along with the work of sociologist Maurizio Meloni (see his Google Scholar page), specifically his book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics. If he did, Coyne would then see that his rebuttal to Ward makes no sense as Baedke discusses epigenetics from an evolutionary perspective and Meloni discusses epigenetics through a social, human perspective and what can—and does—occur in regard to epigenetic processes in humans.
Coyne did discuss Noble’s views on epigenetics and evolution—and Noble responded in one of his talks. However, it seems like Coyne is not aware of the work of Baedke and Meloni—I wonder what he’d say about their work? Anything that attacks the neo-Darwinian Modern Synthesis gets under Coyne’s skin—almost as if it is a religion for him.
Did I like the book? I thought it was good. Out of 5 stars, I give it 3. He got some things wrong, For instance, I asked Shea Robinson, author of Epigenetics and Public Policy: The Tangled Web of Science and Politics about the beginning of the book and he directed me to two articles on his website: Lamarck’s Actual Lamarckism (or How Contemporary Epigenetics is not Lamarckian) and The Unfortunate Legacy of Jean-Baptiste Lamarck. The beginning of the book is rocky, the middle is good (discussing the Cambrian explosion) and the end is alright. The strength of the book is how Ward discusses the processes that epigenetics occurs by and how epigenetic processes can occur—and help drive—evolutionary change, just as Jablonka and Lamb (1995, 2005) argue, along with Baedke (2018). The book is a great read, if only for the history of epigenetics (which Robinson (2018) goes into more depth, as does Baedke (2018) and Meloni (2019)).
Lamarck’s Revenge is a welcome addition to the slew of books and articles that go against the Modern Synthesis and should be required reading for those interested in the history of biology and evolution.
Evolutionary “Progress”: Gould’s Full House Argument
1600 words
Wind back the tape of life to the origin of modern multicellular animals in the Cambrian explosion, let the tape play again from this identical starting point, and the replay will populate the earth (and generate a right tail of life) with a radically different set of creatures. The chance that this alternative set will contain anything remotely like a human being must be effectively nil, while the probability of any kind of creature endowed with self‐consciousness must also be extremely small. (Gould, 1996. Full House)
Wind back the tape of life to the early days of the Burgess Shale; let it play again from an identical starting point, and the chance becomes vanishingly small that anything like human intelligence would grace the replay. (Gould, 1987. Wonderful Life)
Wind back the clock to Cambrian times, half a billion years ago, when mammals first exploded into the fossil record, and let it play forwards again. Would that parallel be similar to our own? Perhaps the hills would be crawling with giant terrestrial octopuses. (Lane, 2015: 21. The Vital Question)
I first read Full House (Gould, 1996) about two years ago. I never was one to believe in evolutionary “progress”, though. As I read through the book, seeing how Gould weaved his love for baseball into an argument against evolutionary “progress” enthralled me. I love baseball, I love evolution, so this was the perfect book for me (indeed, one of my favorite books I have read in my life—and I have read a lot of them). The basic argument goes like this: There are more bacteria on earth than other animals deemed more “advanced”; if evolutionary “progress”—as popularly believed— were true, then there would be more “advanced” mammals than bacteria; there are more bacteria (“simpler: animals) than mammals (more “advanced” animals); therefore evolutionary “progress” is an illusion.
Evolutionary “progress” is entrenched in our society, as can be seen from popular accounts of human evolution (see picture below):
This is the type of “progress” that permeates the minds of the public at large.
Some may look at the diversity of life and conclude that there is a type of “progress” to evolution. However, Gould dispatches with this type of assertion with his drunkard argument. Imagine a drunkard leaving the bar. There is the bar wall (the left wall of complexity) and the gutter (the right wall of complexity). As the drunkard walks, he may stumble in between the left wall and the gutter, but he will always end up in the gutter every time.
Gould explains then explains his reasoning for using this type of argument:
I bring up this old example to illustrate but one salient point: In a system of linear motion structurally constrained by a wall at one end, random movement, with no preferred directionality whatever, will inevitably propel the average position away from a starting point at the wall. The drunkard falls into the gutter every time, but his motion includes no trend whatever toward this form of perdition. Similarly, some average or extreme measure of life might move in a particular direction even if no evolutionary advantage, and no inherent trend, favor that pathway (Gould, 1996: 151).
The claim that there is a type of “progress” to evolution is only due to the fact—in my opinion—that humans exist and are the most “advanced” species on earth.
It seems that JP Rushton did not read this critique of evolutionary “progress”, since not even a year after Gould published Full House, Rushton published anew edition of Race, Evolution, and Behavior (Rushton, 1997) where Rushton argues (on pages 292-294) that there is, indeed, “progress” to evolution. He cites Aristotle, Darwin (1859), Wilson (1975) Russell (1983, 1989; read my critique of Russel’s theory), and Bonner.
To be brief:
The Great Chain of Being (which Rushton’s r/K selection theory attempts to revive) is not valid; Wilson’s idea of “biological progression” is taken care of by Gould’s drunkard argument; Bonner asks why there has been evolution from simple to advanced, and this, too, is taken care of by Gould’s drunkard argument, and finally Dale Russel’s argument about the troodon (I will expand on this below).
Rushton claims that Russell, in his 1989 book Odysseys in Time: Dinosaurs of North America (which I bought specifically to get more info on Russel’s thoughts on the matter and to get more information for an article on it) that “if [dinosaurs] had not gone extinct, dinosaurs would have progressed to a large-brained, bipedal descendent” (Rushton, 1997: 294). Either Rushton only glanced at Russel’s writings or he’s being inherently dishonest: Russel claimed that had the dinosaurs not gone extinct, one dinosaur—the troodon—would have evolved into a bipedal, human-like being. Russel made these claims since the troodon had EQs about 6 times the size of the average dinosaur and they ran on two legs and had use of their ‘hands.’ So, due to this, Russel argues that had the dinosaurs not gone extinct, the troodons could possibly have been human-like. However, there are two huge problems for this hypothesis.
In the book Up From Dragons, Skoyles and Sagan (2002: 12) write:
But cold-bloodedness is a dead-end for the great story of this book—the evolution of intelligence. Certainly reptiles could evolve huge sizes, as they did over vast sweeps of Earth as dinosaurs. But they never could have evolved our quick-witted and smart brains. Being tied to the sun restricts their behavior: Instead of being free and active, searching and understanding the world, they spend too much time avoiding getting too hot or too cold.
So, since dinosaurs are cold-blooded and being tied to the sun restricts their behavior, if they would have survived the K-T extinction event, then it is highly implausible that they would have grown brains our size.
Furthermore, Hopson (1977: 444) writes:
I would argue, as does Feduccia (44), that the mammalian/avian levels of activity claimed by Bakker for dinosaurs should be correlated with a great increase in motor and sensory control and this should be reflected in increased brain size. Such an increase is not indicated by most dinosaur endocasts.
Gould even writes in Wonderful Life:
If mammals had arisen late and helped to drive dinosaurs to their doom, then we could legitimately propose a scenario of expected progress. But dinosaurs remained dominant and probably became extinct only as a quirky result of the most unpredictable of all events—a mass dying triggered by extraterrestrial impact. If dinosaurs had not died in this event, they would probably still dominate the large-bodied vertebrates, as they had for so long with such conspicuous success, and mammals would still be small creatures in the interstices of their world. This situation prevailed for one hundred million years, why not sixty million more? Since dinosaurs were not moving towards markedly larger brains, and since such a prospect may lay outside the capability of reptilian design (Jerison, 1973; Hopson, 1977), we must assume that consciousness would not have evolved on our planet if a cosmic catastrophe had not claimed the dinosaurs as victims. In an entirely literal sense, we owe our existence, as large reasoning mammals, to our lucky stars. (Gould, 1989: 318)
I really don’t think it’s possible that brains our size would have evolved had the dinosaurs not gone extinct, and the data we have about dinosaurs strongly points to that assertion.
Staying on the topic of progression and brain size, there is one more thing I want to note. Deacon (1990a) argues that fallacies exist in the assertion that brain size progressed throughout evolutionary history. One of Deacon’s fallacies is the “evolutionary progression fallacy.” The concept of “progress” finds refuge “implicit expression in the analysis of brain-size differences and presumed grade shifts in allometric brain/body size trends, in theories of comparative intelligence, in claims about the relative proportions of presumed advanced vs. primitive brain areas, in estimates of neural complexity, including the multiplication and differentiation of brain areas, and in the assessment of other species with respect to humans, as the presumed most advanced exemplar” (Deacon, 1990a: 195).
This, in my opinion, is the last refuge for progressionists: looking at the apparent rise of brain size in evolutionary history and saying “Aha! There it is—progress!” So, the so-called progress in brain size evolution is only due to allometric processes, there is no true “progress” in brain size, no unbiased allometric baseline exists, therefore these types of claims from progressionists fail. Lastly, Deacon (1990b) argues that so-called brain size progress vanishes when functional specialization is taken into account.
Therefore it is unlikely that dinosaurs would have evolved brains our size.
In sum, there are many ways that progressionists attempt to show that there is “progress” in evolution. However, they all fail since Gould’s argument is always waiting to rear its head. Yes, some organisms have evolved greater complexity—i.e., moved toward the right wall—though this is not evidence for “progress.” Many—if not all—accounts of “progress” fail. There is no “progress” in brain size evolution; there would not be human-like dinosaurs had the dinosaurs not gone extinct in the K-T extinction event. We live on a planet of bacteria, and since we live on a planet of bacteria—that is, since bacteria are the most numerous type of organism on earth, evolutionary progress cannot be true.
Complexity—getting to the right wall—is an inevitability, just as it is an inevitability that the drunkard would eventually stumble to the gutter. But this does not mean that there is “progress” to evolution.
The argument in Gould’s Full House can be simply stated like this:
P1 The claim that evolutionary “progress” is real and not illusory can only be justified iff organisms deemed more “advanced” outnumber “lesser” organisms.
P2 There are more “lesser” organisms (bacteria/insects) on earth than “advanced” organisms (mammals/species of mammals).
C Therefore evolutionary “progress” is illusory.
NotPoliticallyCorrect 