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Introduction

Cope’s rule is an evolutionary hypothesis which suggests that, over geological time, species have a tendency to increase in body size. (Although it has been proposed for Cope’s rule to be named Deperet’s rule, since Cope didn’t explicitly state the hypothesis while Deperet did, Bokma et al, 2015.) Named after Edward Drinker Cope, it proposes that on average through the process of “natural selection” species have a tendency to get larger, and so it implies a directionality to evolution (Hone and Benton, 2005; Liow and Taylor, 2019). So there are a few explanations for the so-called rule: Either it’s due to passive or driven evolution (McShea, 1994; Gould, 1996; Raia et al, 2012) or due to methodological artifacts (Sowe and Wang, 2008; Monroe and Bokma, 2010).

However, Cope’s rule has been subject to debate and scrutiny in paleontology and evolutionary biology. The interpretation of Cope’s rule hinges on how “body size” is interpreted (mass or length), along with alternative explanations. I will trace the history of Cope’s rule, discuss studies in which it was proposed that this directionality from the rule was empirically shown, discuss methodological issues. I propose alternative explanations that don’t rely on the claim that evolution is “progressive” or “driven.” I will also show that developmental plasticity throws a wrench in this claim, too. I will then end with a constructive dilemma argument showing that either Cope’s rule is a methodological artifact, or it’s due to passive evolution, since it’s not a driven trend as progressionists claim.

How developmental plasticity refutes the concept of “more evolved”

In my last article on this issue, I showed the logical fallacies inherent in the argument PumpkinPerson uses—it affirms the consequent, assuming it’s true leads to a logical contradiction, and of course reading phylogenies in the way he does just isn’t valid.

If the claim “more speciation events within a given taxon = more evolution” were valid, then we would consistently observe a direct correlation between the number of speciation events and the extent evolutionary change in all cases, but we don’t since evolutionary rates vary and other factors influence evolution, so the claim isn’t universally valid.

Take these specific examples: The horseshoe crab has a lineage going back hundreds of millions of years with few speciation events but it has undergone evolutionary changes. Consequently, microorganisms could undergo many speciation events and have relatively minor genetic change. Genetic and phenotypic diversity of the cichlid fishes (fishes that have undergone rapid evolutionary change and speciation), but the diversity between them doesn’t solely depend on speciation events, since factors like ecological niche partitioning and sexual selection also play a role in why they are different even though they are relatively young species (a specific claim that Herculano-Houzel made in her 2016 book The Human Advantage). Lastly, human evolution has relatively few speciation events but the extent of evolutionary change in our species is vast. Speciation events are of course crucial to evolution. But if one reads too much into the abstractness of the evolutionary tree then they will not read it correctly. The position of the terminal nodes is meaningless.

It’s important to realize that evolution just isn’t morphological change which then leads to the creation of a new species (this is macro-evolution), but there is also micro-evolution. Species that underwent evolutionary change without speciation include peppered moths, antibody resistance in bacteria, lactase persistence in humans, Darwin’s finches, and industrial melanism in moths. These are quite clearly evolutionary changes, and they’re due to microevolutionary changes.

Developmental plasticity directly refutes the contention of more evolved since individuals within a species can exhibit significant trait variation without speciation events. This isn’t captured by phylogenies. They’re typically modeled on genetic data and they don’t capture developmental differences that arise due to environmental factors during development. (See West-Eberhard’outstanding Developmental Plasticity and Evolution for more on how in many cases development precedes genetic change, meaning that the inference can be drawn that genes aren’t leaders in evolution, they’re mere followers.)

If “more evolved” is solely determined by the number of speciation events (branches) in a phylogeny, then species that exhibit greater developmental plasticity should be considered “more evolved.” But it is empirically observed that some species exhibit significant developmental plasticity which allows them to rapidly change their traits during development in response to environmental variation without undergoing speciation. So since the species with more developmental plasticity aren’t considered “more evolved” based on the “more evolved” criteria, then the assumption that “more evolved” is determined by speciation events is invalid. So the concept of “more evolved” as determined by speciation events or branches isn’t valid since it isn’t supported when considering the significant role of developmental plasticity in adaptation.

There is anagenesis and cladogenesis. Anagenesis is the creation of a species without a branching of the ancestral species. Cladogenesis is the formation of a new species by evolutionary divergence from an ancestral form. So due to evolutionary changes within a lineage, the organism that underwent evolutionary changes replaces the older one. So anagenesis shows that a species can slowly change and become a new species without there being a branching event. Horse, human, elephant, and bird evolution are examples of this.

Nonetheless, developmental plasticity can lead to anagenesis. Developmental, or phenotypic, plasticity is the ability of an organism to produce different phenotypes with the same genotype based on environmental cues that occur during development. Developmental plasticity can facilitate anagenesis, and since developmental plasticity is ubiquitous in development of not only an individual in a species but a species as a whole, then it is a rule and not an exception.

Directed mutation and evolution

Back in March, I wrote on the existence of directed mutations. Directed mutation directly speaks against the concept of “more evolved.” Here’s the argument:

(1) If directed mutations play a crucial role in helping organisms adapt to changing environments, then the notion of “more evolved” as a linear hierarchy is invalid.
(2) Directed mutations are known to occur and contribute to a species survivability in an environment undergoing change during development (the concept of evolvability is apt here).
(C) So the concept of “more evolved” as a linear hierarchy is invalid.

A directed mutation is a mutation that occurs due to environmental instability which helps an organism survive in the environment that changed while the individual was developing. Two mechanisms of DM are transcriptional activation (TA) and supercoiling. TAs can cause changes to single-stranded DNA, and can also cause supercoiling (the addition of more strands on DNA). TA can be caused by depression (a mechanism that occurs due to the absence of some molecule) or induction (the activation of an inactive gene which then gets transcribed). So these are examples of how nonrandom (directed) mutation and evolution can occur (Wright, 2000). Such changes are possibly through the plasticity of phenotypes during development and ultimately are due to developmental plasticity. These stress-directed mutations can be seen as quasi-Lamarckian (Koonin and Wolf, 2009). It’s quite clear that directed mutations are a thing and have been proven true.

DMs, along with developmental plasticity and evo-devo as a whole refute the simplistic thinking of “more evolved.”

Now here is the argument that PP is using, and why it’s false:

(1) More branches on a phylogeny indicate more speciation events.
(2) More speciation events imply a higher level of evolutionary advancement.
(C) Thus, more branches on a phylogeny indicate a higher level of evolutionary advancement.

The false premise is (2) since it suggests that more speciation events imply a higher level of evolutionary advancement. It implies a goal-directed aspect to evolution, where the generation of more species is equated with evolutionary progress. It’s just reducing evolution to linear advancement and progress; it’s a teleological bent on evolution (which isn’t inherently bad if argued for correctly, see Noble and Noble, 2022). But using mere branching events on a phylogeny to assume that more branches = more speciation = more evolved is simplistic thinking that doesn’t make sense.

If evolution encompasses changes in an organism’s phenotype, then changes in an organism’s phenotype, even without changing its genes, are considered examples of evolution. Evolution encompasses changes in an organism’s phenotype, so changes in an organism’s phenotype even without changes in genes are considered examples of evolution. There is nongenetic “soft inheritance” (see Bonduriansky and Day, 2018).

Organisms can exhibit similar traits due to convergent evolution. So it’s not valid to assume a direct and strong correlation between and organism’s position on a phylogeny and it’s degree of resemblance to a common ancestor.

Dolphins and ichthyosaurs share similar traits but dolphins are mammals while ichthyosaurs are reptiles that lived millions of years ago. Their convergent morphology demonstrates that common ancestry doesn’t determine resemblance. The Tasmanian and Grey wolf have independently evolved similar body plans and roles in their ecologies and despite different genetics and evolutionary history, they share a physical resemblance due to similar ecological niches. The LCA of bats and birds didn’t have wings but they have wings and they occurred independently showing that the trait emerged independently while the LCA didn’t have wings so it emerged twice independently. These examples show that the degree of resemblance to a common ancestor is not determined by an organism’s position on a phylogeny.

Now, there is a correlation between body size and branches (splits) on a phylogeny (Cope’s rule) and I will explain that later. That there is a correlation doesn’t mean that there is a linear progression and they don’t imply a linear progression. Years ago back in 2017 I used the example of floresiensis and that holds here too. And Terrance Deacon’s (1990) work suggests that pseudoprogressive trends in brain size can be explained by bigger whole organisms being selected—this is important because the whole animal is selected, not any one of its individual parts. The correlation isn’t indicative of a linear progression up some evolutionary ladder, either: It’s merely a byproduct of selecting larger animals (the only things that are selected).

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, 1990)

Nonetheless, the claim here is one from DST—the whole organism is selected, so obviously so is it’s body plan (bauplan). Nevertheless, the last two havens for the progressionist is in the realm of brain size and body size. Deacon refuted the selection-for brain size claim, so we’re now left with body size.

Does the evolution of body size lend credence to claims of driven, progressive evolution?

The tendency for bodies to grow larger and larger over evolutionary time is something of a trusim. Since smaller bacterium have eventually evolved into larger (see Gould’s modal bacter argument), more complex multicellular organisms, then this must mean that evolution is progressive and driven, at least for body size, right? Wrong. I will argue here using a constructive dilemma that either evolution is passive and that’s what explains the evolution of body size increases, or is it due to methodological flaws in how body size is measured (length or mass)?

In Full House, Gould (1996) argued that the evolution of body size isn’t driven, but that it is passive, namely that it is evolution away from smaller size. Nonetheless, it seems that Cope’s (Deperet’s) rule is due to cladogenesis (the emergence of new species), not selection for body size per se (Bokma et al, 2015).

Given these three conditions, we note an increase in size of the largest species only because founding species start at the left wall, and the range of size can therefore expand in only one direction. Size of the most common species (the modal decade) never changes, and descendants show no bias for arising at larger sizes than ancestors. But, during each act, the range of size expands in the only open direction by increase in the total number of species, a few of which (and only a few) become larger (while none can penetrate the left wall and get smaller). We can say only this for Cope’s Rule: in cases with boundary conditions like the three listed above, extreme achievements in body size will move away from initial values near walls. Size increase, in other words, is really random evolution away from small size, not directed evolution toward large size. (Gould, 1996)

Dinosaurs were some of the largest animals to ever live. So we might say that there is a drivenness in their bodies to become larger and larger, right? Wrong. The evolution of body size in dinosaurs is passive, not driven (progressive) (Sookias, Butler, and Benson, 2012). Gould (1996) also showed passive trends in body size in plankton and forams. He also cited Stanley (1973) who argued that groups starting at the left wall of minimum complexity will increase in mean size as a consequence of randomness, not any driven tendency for larger body size.

In other, more legitimate cases, increases in means or extremes occur, as in our story of planktonic forams, because lineages started near the left wall of a potential range in size and then filled available space as the number of species increased—in other words, a drift of means or extremes away from a small size, rather than directed evolution of lineages toward large size (and remember that such a drift can occur within a regime of random change in size for each individual lineage—the “drunkard’s walk” model).

In 1973, my colleague Steven Stanley of Johns Hopkins University published a marvelous, and now celebrated, paper to advance this important argument. He showed (see Figure 27, taken from his work) that groups beginning at small size, and constrained by a left wall near this starting point, will increase in mean or extreme size under a regime of random evolution within each species. He also advocated that we test his idea by looking for right-skewed distributions of size within entire systems, rather than by tracking mean or extreme values that falsely abstract such systems as single numbers. In a 1985 paper I suggested that we speak of “Stanley’s Rule” when such an increase of means or extremes can best be explained by undirected evolution away from a starting point near a left wall. I would venture to guess (in fact I would wager substantial money on the proposition) that a large majority of lineages showing increase of body size for mean or extreme values (Cope’s Rule in the broad sense) will properly be explained by Stanley’s Rule of random evolution away from small size rather than by the conventional account of directed evolution toward selectively advantageous large size. (Gould, 1996)

Gould (1996) also discusses the results of McShea’s study, writing:

Passive trends (see Figure 33) conform to the unfamiliar model, championed for complexity in this book, of overall results arising as incidental consequences, with no favored direction for individual species, (McShea calls such a trend passive because no driver conducts any species along a preferred pathway. The general trend will arise even when the evolution of each individual species confirms to a “drunkard’s walk” of random motion.) For passive trends in complexity, McShea proposes the same set of constraints that I have advocated throughout this book: ancestral beginnings at a left wall of minimal complexity, with only one direction open to novelty in subsequent evolution.

But Baker et al (2015) claim that body size is an example of driven evolution. However, that they did not model cladogenetic factors calls their conclusion into question. But I think Baker et al’s claim doesn’t follow. If a taxon possesses a potential size range and the ancestral size approaches the lower limit of this range, it will result in a passive inclination for descendants to exceed the size of their ancestors. The taxon in question possesses a potential size range, and the ancestral size range is on the lower end of the range. So there will be a passive tendency for descendants of this taxon to be larger than their predecessors.

Here’s an argument that concludes that evolution is passive and not driven. I will then give examples of P2.

(1) Extant animals that are descended from more nodes on an evolutionary tree tend to be bigger than animals descended from fewer nodes (your initial premise).
(2) There exist cases where extant animals descended from fewer nodes are larger or more complex than those descended from more nodes (counterexamples of bats and whales, whales are descended from fewer nodes while having some of the largest body sizes in the world while bats are descended from more nodes while having a way comparatively smaller body size).
(C1) Thus, either P1 doesn’t consistently hold (not all extant animals descended from more nodes are larger), or it is not a reliable rule (given the counters).
(3) If P1 does not consistently hold true (not all extant animals descended from more nodes are larger), then it is not a reliable rule.
(4) P1 does not consistently hold true.
(C2) P1 is not a reliable rule.
(5) If P1 is not a reliable rule (given the existence of counterexamples), then it is not a valid generalization.
(6) P1 is not a reliable rule.
(C3) So P1 is not a valid generalization.
(6) If P1 isn’t a valid generalization in the context of evolutionary biology, then there must be exceptions to this observed trend.
(7) The existence of passive evolution, as suggested by the inconsistenties in P1, implies that the trends aren’t driven by progressive forces.
(C4) Thus, the presence of passive evolution and exceptions to P1’s trend challenge the notion of a universally progressive model of evolution.
(8) If the presence of passive evolution and exceptions to P1’s trend challenges the notion of a universally progressive model of evolution, then the notion of a universally progressive model of evolution isn’t supported by the evidence, as indicated by passive evolution and exceptions to P1’s trend.
(9) The presence of passive evolution and exceptions to P1’s trend challenge the notion. of a universally progressive model of evolution.

(1) Bluefin tuna are known to have a potential range of size, with some being small and others being massive (think of that TV show Deadliest Catch and the massive size ranges of tuna these fisherman catch, both in length and mass). So imagine a population of bluefin tuna where the ancestral size is found to be close to the lower end of their size range. So P2 is satisfied because bluefin tuna have a potential size range. So the ancestral size of the ancestors of the tuna were relatively small in comparison to the maximum size of the tuna.

(2) African elephants in some parts of Africa are small, due to ecological constraints and hunting pressures and these smaller-sized ancestors are close to the lower limit of the potential size range of African elephants. Thus, according to P1, there will be a passive tendency for descendants of these elephants to be larger than their smaller-sizes ancestors over time.

(3) Consider galapagos tortoises whom are also known for their large variation in size among the different species and populations on the galapagos islands. So consider a case of galapagos tortoises who have smaller body sizes due to either resource conditions or the conditions of their ecologies. So in this case, the potential size for the ancestors of these tortoises is close to the theoretical limit of their potential size range. Therefore, we can expect a passive tendency for descendants of these tortoises to evolve large body sizes.

Further, in Stanley’s (1973) study of Cope’s rule from fossil rodents, he observed that body size distributions in these rodents, over time, became bigger while the modal size stayed small. This doesn’t even touch the fact that because there are more small than large mammals, that there would be a passive tendency in large body sizes for mammals. This also doesn’t even touch the methodological issues in determining body size for the rule—mass, length? Nonetheless, Monroe and Bokma’s (2010) study showed that while there is a tendency for species to be larger than their ancestors, it was a mere 0.5 percent difference. So the increase in body size is explained by an increase in variance in body size (passiveness) not drivenness.

Explaining the rule

I think there are two explanations: Either a methodological artifact or passive evolution. I will discuss both, and I will then give a constructive dilemma argument that articulates this position.

Monroe and Bokma (2010) showed that even when Cope’s rule is assumed, the ancestor-descendant increase in body size showed a mere .4 percent increase. They further discussed methodological issues with the so-called rule, citing Solow and Wang (2008) who showed that Cope’s rule “appears” based on what assumptions of body size are used. For example, Monroe and Bokma (2010) write:

If Cope’s rule is interpreted as an increase in the mean size of lineages, it is for example possible that body mass suggests Cope’s rule whereas body length does not. If Cope’s rule is instead interpreted as an increase in the median body size of a lineage, its validity may depend on the number of speciation events separating an ancestor-descendant pair.

…

If size increase were a general property of evolutionary lineages – as Cope’s rule suggests – then even if its effect were only moderate, 120 years of research would probably have yielded more convincing and widespread evidence than we have seen so far.

Gould (1997) suggested that Cope’s rule is a mere psychological artifact. But I think it’s deeper than that. Now I will provide my constructive dilemma argument, now that I have ruled out body size being due to progressive, driven evolution.

The form of constructive dilemma goes: (1) A V B. (2) If A, then C. (3) If B, then D. (C) C V D. P1 represents a disjunction: There are two possible choices, A and B. P2 and P3 are conditional statements, that provide implications for both of the options. And C states that at least one or both of the implications have to be true (C or D).

Now, Gould’s Full House argument can be formulated either using modus tollens or constructive dillema:

(1) If evolution were a deterministic, teleological process, there would be a clear overall progression and a predetermined endpoint. (2) There is no predetermined endpoint or progression to evolution. (C) So evolution isn’t a deterministic or teleological process.

(1) Either evolution is a deterministic, teleological process (A) or it’s not (B). (2) If A, then there would be a clear direction and predetermined endpoint. (3) If B, then there is no overall direction or predetermined endpoint. (4) So either there is a clear overall progression (A), or there isn’t (B). (5) Not A. (6) Therefore, B.

Or (1) Life began at a relatively simple state (the left wall of complexity). (2) Evolution is influenced by a combination of chance events,, environmental factors and genetic variation. (3) Organisms may stumble I’m various directions along the path of evolution. (4) Evolution lacks a clear path or predetermined endpoint.

Now here is the overall argument combining the methodological issues pointed out by Sowe and Wang and the implications of passive evolution, combined with Gould’s Full House argument:

(1) Either Cope’s rule is a methodological artifact (A), or it’s due to passive, not driven evolution (B). (2) If Cope’s rule is a methodological artifact (A), then different ways to measure body size (length or mass) can come to different conclusions. (3) If Cope’s rule is due to passive, not driven evolution (B), then it implies that larger body sizes simply accumulate over time without being actively driven by selective pressures. (4) Either evolution is a deterministic, teleological process (C), or it is not (D). (5) If C, then there would be a clear overall direction and predetermined endpoint in evolution (Gould’s argument). (6) If D, then there is no clear overall direction or predetermined endpoint in evolution (Gould’s argument). (7) Therefore, either there is a clear overall direction (C) or there isn’t (D) (Constructive Dilemma). (8) If there is a clear overall direction (C) in evolution, then it contradicts passive, not driven evolution (B). (9) If there isn’t a clear overall direction (D) in evolution, then it supports passive, not driven evolution (B). (10) Therefore, either Cope’s rule is due to passive evolution or it’s a methodological artifact.

Conclusion

Evolution is quite clearly passive and non-driven (Bonner, 2013). The fact of the matter is, as I’ve shown, evolution isn’t driven (progressive), it is passive due to the drunken, random walk that organisms take from the minimum left wall of complexity. The discussions of developmental plasticity and directed mutation further show that evolution can’t be progressive or driven. Organism body plans had nowhere to go but up from the left wall of minimal complexity, and that means increase the variance in, say, body size is due to passive trends. Given the discussion here, we can draw one main inference: since evolution isn’t directed or progressive, then the so-called Cope’s (Deperet’s) rule is either due to passive trends or they are mere methodological artifacts. The argument I have mounted for that claim is sound and so, it obviously must be accepted that evolution is a random, drunken walk, not one of overall drivenness and progress and so, we must therefore look at the evolution of body size in this way.

Rushton tried to use the concept of evolutionary progress to argue that some races may be “more evolved” than other races, like “Mongoloids” being “more evolved” than “Caucasoids” who are “more evolved” than “Negroids.” But Rushton’s “theory” was merely a racist one, and it obviously fails upon close inspection. Moreover, even the claims Rushton made at the end of his book Race, Evolution, and Behavior don’t even work. (See here.) Evolution isn’t progressive so we can’t logically state that one population group is more “advanced” or “evolved” than another. This is of course merely Rushton being racist with shoddy “explanations” used to justify it. (Like in Rushton’s long-refuted r/K selection theory or Differential-K theory, where more “K-evolved” races are “more advanced” than others.)

Lastly, this argument I constructed based on the principles of Gould’s argument shows that there is no progress to evolution.

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.