Say what you want about the tone of the Graur et al. (2013) paper in Genome Biology and Evolution, but it has people talking. Including Ewan Birney, the lead scientist of the ENCODE project and the primary spokesperson for ENCODE in the media fiasco describing the “death of junk DNA”. Most recently, Birney was interviewed by Quentin Cooper on the BBC Radio 4 program Material World, along with Oxford biologist Chris Ponting. You can listen to the show here.
I have also transcribed the parts in which Birney discusses the ENCODE findings and the flap around the claims of “80% function” of the human genome. Again, remember that Birney himself said several times in prior interviews that the ENCODE results undermine the idea of junk DNA and that the genome is jam packed with “switches” (see here, here, here, and here).
Quentin Cooper (host): Ok, well, Ewan, we’ll get on to what this paper says and doesn’t say, but can you just give us a quick precis of why ENCODE’s findings are in such contrast to a lot of conventional thinking and clearly a lot of current thinking about junk DNA?
Ewan Birney (Lead scientist, ENCODE): I don’t think the findings are in such stark contrast. It’s more about the interpretation of the words, in particular when the words get used in, um, out of context, out of the scientific paper context and propagated. So, what exactly do we mean by this word “junk”?.
Quentin Cooper: But are you sure it’s all about the context. Because I mean, one of the reasons why these findings attracted so much interest was because it didn’t seem to fit the conventional thinking. It can’t just be down to a bit of phraseology and saying actually confirms what we already knew, can it?
Ewan Birney: Ah, so, I don’t — It’s interesting to reflect back on this. For me, the big important thing of ENCODE is that we found that a lot of the genome had some kind of biochemical activity. And we do describe that as “biochemical function”, but that word “function” in the phrase “biochemical function”is the thing which gets confusing. If we use the phrase “biochemical activity”, that’s precisely what we did, we find that the different parts of the genome, [??] 80% have some specific biochemical event we can attach to it. I was often asked whether that 80% goes to 100%, and that’s what I believe it will do. So, in other words, that number is much more about the coverage of what we’ve assayed over the entire genome. In the paper, we say quite clearly that the majority of the genome is not under negative selection, and we say that most of the elements are not under pan-mammalian selection. So that’s negative selection we can detect between lots of different
mammals. [??} really interesting question about what is precisely going on in the human population, but that’s — you know, I’m much closer to the instincts of this kind of 10% to 20% sort of range about what is under, sort of what evolution cares about under selection.
Quentin Cooper: But this paper that’s appeared in the journal Genome Biology and Evolution, Dan Graur from the University of Texas, professor there, all these lines, do you think they’re reacting more to the press coverage around the story rather than what’s actually in your paper itself?
Ewan Birney: That’s my belief. And of course in some sense our responsibility to help that press coverage do the right thing and that’s what I worked very hard in September, in particular in the UK context where I’m based, to try and make that press coverage work. It is quite complicated, because you want to be excited about what you’re doing, but you don’t want people to get the wrong — draw the wrong interpretation of it. So, it’s not an easy job to do, but I believe that most of the heat in this debate is about the definitions of the words, and not the data or the interpretation of the data.
Chris Ponting (Oxford University): Ewan, my question to you is, how much of the genome do you think is vital for life?
Ewan Birney: Yeah, I don’t, I would do that on a, as you know I’ve blogged about this. You know, certainly everything that’s under negative selection in the human population, that evolution cares about right now in humans, that if it changes then the person has less reproductive fitness, that’s clearly vital for life. I think there is a chance of there being a small amount of additional things that we find interesting about differences between people that are not under selection. So, those may be phenotypes that are late-onset such as neurodegenerative diseases or things like that. So, I think there’s a little addition to that but those are the kind of boundary components to that.
Chris Ponting: So I think we can probably agree between us that between 10% and say 20% is vital for life.
Ewan Birney: I mean, I think we would agree with that. I think, you know, refining that percentage down is quite interesting. I think also the other components that we — biochemical events that we see in the genome, sort of, each one of them are equally likely to be part of that 10% to 20% that we’re looking for. It’s important to realize that it’s not the case that we can spot the 10% to 20% just by looking harder. Each of these different places in the genome that have some biochemical activity associated with it, when there’s some phenotype screen that’s directed there or some evolutionary screen that’s directed to that point, ENCODE can now say “Ah ha! Here is a biochemical thing that this piece of DNA looks like it could be doing”.
Quentin Cooper: Ewan, just briefly, what about another aspect of the criticism, the idea that the ENCODE project lacked anyone with any real knowledge of evolutionary biology?
Ewan Birney: Well, I’m sure we could have, um, ahhh, had, um, many other people join us. There were a number of us who have worked — I do know quite a bit about evolutionary biology. Whether everybody considers me to be an expert, I don’t, you know, that’s for other people to say. If you read the paper, and not the press reports, there is a lot detail spent on what is under different aspects of evolutionary biology, ah, selection. So, I think again, a lot of this is not about the paper, but is more about the words used to describe the paper.
Quentin Cooper: Finally though, Ewan, is there any of the criticism you do take on the chin, think well perhaps we did let the story get a bit away from us at times?
Ewan Birney: Well, hindsight is a fairly cruel thing. And one of the things which I regret about being in this situation, arguing about words in the press, is I just wish there was a way of us not talking about this. I think ENCODE already is being used by many, many different groups, in particular disease biology groups having their phenotypes screened against it, and other people worldwide. And the whole point of this for the data by the project to be used by many, many other groups. I’m really happy about that, um, and hindsight being such a cruel thing, makes me think about what I could have done to minimize this kind of rather heated debate.
I expect that we will be seeing several harsh critiques of ENCODE’s extraordinary claims about function in the human genome and the equally incredible mega-hype associated with the project. I know of at least one more that is forthcoming from a heavy-hitter in the field, but as a snarky smackdown, it will be very tough to beat the recent paper by Dan Graur and colleagues published in Genome Biology and Evolution. The paper is open-access, so go ahead and read it yourself here. Meantime, enjoy the following zingers:
ENCODE adopted a strong version of the causal role definition of function, according to which a functional element is a discrete genome segment that produces a protein or an RNA or displays a reproducible biochemical signature (for example, protein binding).
Oddly, ENCODE not only uses the wrong concept of functionality, it uses it wrongly and inconsistently.
…the ENCODE authors singled out transcription as a function, as if the passage of RNA polymerase through a DNA sequence is in some way more meaningful than other functions. But, what about DNA polymerase and DNA replication? Why make a big fuss about 74.7% of the genome that is transcribed, and yet ignore the fact that 100% of the genome takes part in a strikingly “reproducible biochemical signature”—it replicates!
Ward and Kellis (2012) confirmed that ~5% of the genome is interspecifically conserved, and by using intraspecific variation, found evidence of lineage-specific constraint suggesting that an additional 4% of the human genome is under selection (i.e., functional), bringing the total fraction of the genome that is certain to be functional to approximately 9%. The journal Science used this value to proclaim “No More Junk DNA” Hurtley 2012), thus, in effect rounding up 9% to 100%.
ENCODE chose to bias its results by excessively favoring sensitivity over specificity. In fact, they could have saved millions of dollars and many thousands of research hours by ignoring selectivity altogether, and proclaiming a priori that 100% of the genome is functional. Not one functional element would have been missed by using this procedure.
Interestingly, ENCODE, which is otherwise quite miserly in spelling out the exact function of its “functional” elements, provides putative functions for each of its 12 histone modifications. For example, according to ENCODE, the putative function of the H4K20me1 modification is “preference for 5’ end of genes.” This is akin to asserting that the function of the White House is to occupy the lot of land at the 1600 block of Pennsylvania Avenue in Washington, D.C.
In a miraculous feat of “next generation” science, the ENCODE authors were able to determine the frequencies of nonexistent derived alleles.
… a surprisingly large number of scientists have had their knickers in a twist over “junk DNA” ever since the term was coined by Susumu Ohno (1972).
In dissecting common objections to “junk DNA,” we identified several misconceptions, chief among them (1) a lack of knowledge of the original and correct sense of the term, (2) the belief that evolution can always get rid of nonfunctional DNA, and (3) the belief that “future potential” constitutes “a function.”
We urge biologists not be afraid of junk DNA. The only people that should be afraid are those claiming that natural processes are insufficient to explain life and that evolutionary theory should be supplemented or supplanted by an intelligent designer (e.g., Dembski
1998; Wells 2004). ENCODE’s take-home message that everything has a function implies purpose, and purpose is the only thing that evolution cannot provide. Needless to say, in light of our investigation of the ENCODE publication, it is safe to state that the news concerning the death of “junk DNA” have been greatly exaggerated.
ENCODE’s biggest scientific sin was not being satisfied with its role as data provider; it assumed the small-science role of interpreter of the data, thereby performing a kind of textual hermeneutics on a 3.5-billion-long DNA text. Unfortunately, ENCODE disregarded the rules of scientific interpretation and adopted a position common to many types of theological hermeneutics, whereby every letter in a text is assumed a priori to have a meaning.
So, what have we learned from the efforts of 442 researchers consuming 288 million dollars? According to Eric Lander, a Human Genome Project luminary, ENCODE is the “Google Maps of the human genome” (Durbin et al. 2010). We beg to differ, ENCODE is considerably worse than even Apple Maps.
We conclude that the ENCODE Consortium has, so far, failed to provide a compelling reason to abandon the prevailing understanding among evolutionary biologists according to which most of the human genome is devoid of function. The ENCODE results were
predicted by one of its lead authors to necessitate the rewriting of textbooks (Pennisi 2012). We agree, many textbooks dealing with marketing, mass-media hype, and public relations may well have to be rewritten.
I’ll just let this soup sandwich of an abstract speak for itself:
We find that the global relationships among species should be of circular phylogeny, which is quite different from common sense based on phylogenetic trees. A domain can be defined by a distinct phylogenetic circle, which is a global and stable characteristic of the living system. The mechanism in genome size evolution has been clarified; hence the main component questions on C-value enigma can be explained. We find the intrinsic relationship between genome size evolution and protein length evolution; that is the genome size and non-coding DNA ratio can be calculated based on protein length distributions.
(These are the same authors who brought us thisturd gem).
In the paper, Gould and Lewontin (1979) drew an analogy between the “spandrels” (or, if you’re overly pedantic about architectural terminology, “pendentives“) in Saint Mark’s Basilica in Venice and features of organisms that are often assumed to represent adaptations whose current functions reflect the reason for their origin. The spandrels in St. Mark’s Basilica house elaborate mosaics depicting important Christian iconography, and represent one of the most stunning aspects of the cathedral. However, housing religious imagery is not why the spandrels were created in the first place. As Gould and Lewontin (1979) point out, spandrels are the inevitable result of resting a domed ceiling atop walls with arched doorways. Once they exist, spandrels can be co-opted for a function such as artistic decoration — but whatever this current function may be, it does not, by itself, explain the origin of the structures. Many traits of organisms, rather than being the result of adaptive evolution under selection for their current function (if any) are, in fact, biological “spandrels”.
Yours truly enjoying the amazing artistry in St. Mark’s Basilica.
The tendency to conflate current function with historical origin is one of the things that Gould and Lewontin saw as a pervasive problem in the evolutionary biology of the 1970s. They also considered the general tendency to focus almost exclusively on adaptationist explanations for individual traits to be misguided. Not only did authors not properly consider alternative, non-adaptive explanations, they presented only weak evidence in support of adaptive “just-so stories” or simply moved on to a new adaptive tale if evidence was found lacking for a particular explanation.
An adaptationist programme has dominated evolutionary thought in England and the United States during the past 40 years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary ‘traits’ and proposing an adaptive story for each considered separately. Trade-offs among competing selective demands exert the only brake upon perfection; non-optimality is thereby rendered as a result of adaptation as well. We criticize this approach and attempt to reassert a competing notion (long popular in continental Europe) that organisms must be analysed as integrated wholes, with Bauplane so constrained by phyletic heritage, pathways of development and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. We 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 non-adaptive 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 non-adaptive structures. We support Darwin’s own pluralistic approach to identifying the agents of evolutionary change.
Some subsequent authors have charged that Gould and Lewontin (1979) presented a straw man, and did not provide a fair assessment of what members of the so-called adaptationist camp actually did or said. Nevertheless, I think many biologists feel that theirs was a very important contribution, at least as a warning for how the study of trait evolution could go awry. I would take a stronger position, and argue that not only was the Gould and Lewontin (1979) paper needed at the time, but that it is still needed today. And nowhere is this more true than in studies of human behaviour and anatomy, particularly because these tend to be widely covered in the science media. Evolutionary psychology takes a large amount of flak from evolutionary biologists and others for its perceived tendency to present “just-so stories” or to make extraordinary assumptions about the social and physical habitats of hominin ancestors. But this is not limited to studies of human minds by any means.
I recently discussed one example, the widely-reported claim that the dimensions of human hands evolved in large part to allow the formation of fists. In that post, I outlined several major problems with the underlying assumptions and the (very weak) data that were presented as supporting evidence. I won’t re-hash these points here, but many of them apply equally to the even more recent claim that a human trait is the product of adaptive evolution: namely that the wrinkling of our fingers and toes when submerged in water is an adaptation for gripping in wet conditions.
The idea was first put forward by Mark Changizi and colleagues of 2AI Labs in Boise, Idaho. Changizi has a PhD in applied math and primarily studies neurobiology, but in this case his focus was on why fingers wrinkle when they’re soaked. Specifically, Changizi et al. (2011) wondered whether the wrinkled patterns that form on the fingers after prolonged soaking have a function similar to the treads on tires, namely for channelling water and improving grip in wet conditions. Based on the idea that wrinkled digits might actually represent water channels, they looked at photos of 28 wrinkly fingers from 13 hands that they found online. They then compared these wrinkle patterns to the channels of rivers in a mountainous drainage system and to the treads on car tires and found that they are similar in that they branch and diverge from the middle of the finger.
From Changizi et al. (2011).
From Changizi et al. (2011).
In addition, the authors noted that the wrinkling of fingers is not simply a result of osmotic changes when hands are soaked, and that there is evidence that the process is linked to the action of the autonomic nervous system. Or, at least, wrinkling does not occur if there is nerve damage in the hand. In fact, physicians use wrinkling in water as a test of neural function in the limbs (Wilder-Smith 2004; Barneveld et al. 2010). So, the evidence to this point was a) wrinkling seems to be under nervous control, and b) the wrinkles look like drainage systems or tire treads.
This hypothesis has gained more attention recently with the publication of a follow up study by Kareklas et al. (2013) in the lab of Tom Smulders in the Institute of Neuroscience at Newcastle University. Kareklas et al. (2013) wanted to test the idea that wrinkling improves grip in wet conditions. To do so, they had 20 volunteers soak their hands in 40°C water for 30 minutes and then had them move marbles of different sizes from one container to another, with the source container either filled with water or dry. They compared this to the performance of the volunteers in the same task when their hands had not been soaked and therefore their fingers were not wrinkled.
From Kareklas et al. (2013).
Here is the entire Results section of the paper:
It took participants anywhere between 72 s (fastest person) and 198 s (slowest person) to transfer all the items. All participants transferred dry objects more quickly than submerged objects, taking on average 17 per cent (±2.3% s.e.m.) more time to transfer submerged objects (F1,16 = 35.80, p < 0.001). With wrinkled fingers, transfer of submerged objects happened in 12 per cent (±2.3% s.e.m.) less time than with unwrinkled fingers. There was no difference in the time it took to transfer dry objects with or without wrinkles on the fingers (interaction: F1,16 = 44.10, p < 0.001; figure 1). This finding shows a clear advantage of having wrinkled fingers when manipulating submerged objects, but not dry objects.
In short, soaking your hands in 40°C water for 30 minutes will give you a 12% advantage in picking up round, smooth objects if they are underwater.
Not surprisingly, given that it is about a familiar yet curious human trait, the science media have reported this study widely.
Now, as you may have guessed, I don’t find this hypothesis compelling at all, for many reasons. The first is that it is based on the thinnest of datasets. Photos of 13 hands with finger wrinkles that resemble drainage channels. And a small advantage in manipulating wet marbles. That’s it for the data.
I also don’t buy the conceptual arguments, for example Changizi’s claim that there are infinitely many possible patterns for wrinkles to form, and yet we see the one that is consistent with rain treads. I strongly doubt that there are more than a few possible arrangements for wrinkles, given the properties of human skin and the shape of human digits. Moreover, it looks to me like there is substantial variability in wrinkle patterns even within the tiny sample of their study. Would all of these channel water effectively? We don’t know, because no effort was taken to demonstrate that wrinkles actually displace water. (I have my doubts about this. Treads are hard, fingers are soft. Tires rotate, fingers don’t).
Finally, I am not convinced that the link to the central nervous system implies that this trait is functional. Vasoconstriction is involved (Wilder-Smith and Chow 2003a,b), and this can be controlled by the nervous system, but that alone does not mean that the trait evolved as an adaptation rather than as a spandrel. Perhaps the effect is simply a byproduct of other nerve signal changes that are functional in response to hot water immersion. I don’t know, but neither does anyone else because such non-adaptive hypotheses have not been considered. There certainly seems to be some cross-wiring going on, since reduced wrinkling ability is correlated with congestive heart failure (Kamran et al. 2011) and heart rate variability (Win et al. 2010).
There is also this:
From Reh (1984).
The photo above shows a pretty typical wrinkle pattern for a hand that has been submerged in water (in this case, for 120 minutes in 13°C water). What sets this hand apart from the ones examined by Changizi et al. (2011) is that it belongs to a dead person. That is to say, wrinkling occurs, with the same pattern and at a similar rate, even when the subject is deceased (Weber and Laufkötter 1984; Reh 1984).
From Reh (1984):
Studies were carried out systematically in both corpses and the hands of corpses in order to find out when ” washerwoman ‘s skin” begins. The temperatures ranged between 10 degrees and 18 degrees C and the time of the experiments did not exceed 300 min. The initial formation of washerwoman ‘s skin could be observed after 20-30 min at the fingertips and after 50-60 min in the entire finger. The longest intervals observed were 100 or 150 min, respectively. These long intervals were interpreted as being exceptions from the norm, probably due to either extraordinarily heavy strips of fat on the fingers or abnormally hard skin on the hands. The course of washerwoman ‘s skin obviously depends on the water temperature, and afterwards it disappears rather slowly–even after a short immersion–in the open air. We will carry out additional experiments in the future.
If finger and toe wrinkling is an adaptation for gripping in the wet as claimed, we might also ask:
Why does it take so long to occur? Wouldn’t it be better to have a quick response rather than a system that takes at least a few minutes of immersion to kick in? (I stood in the warm shower for 10 minutes this morning, and my feet did not wrinkle at all.)
Why is the response strongest in very warm water (Cales et al. 1997)? Is 40°C water really encountered a lot under natural conditions of foraging or running?
If this is an adaptation for simply channelling water, why is the response strongly affected by the salinity and pH of the water (Tsai and Kirkham 2005)?
I don’t think these observations provide support for the idea that finger wrinkling is an adaptive response to being wet, or at least they are not what I would expect to be the case if this were such an adaptation.
In any case, the bigger problem with the wrinkled gripper ape hypothesis, the punching ape hypothesis, and other such hypotheses is that they are not based on solid evolutionary thinking. More specifically, the authors of these hypotheses do not seem to work through the assumptions that would have to be true for these traits to be adaptive in the way that they propose. Did an ancestral population actually have variation in this trait, and is it heritable? Did these ancestors really submerge their hands and feet regularly? Did individuals with more wrinkles actually have more children than individuals with less tread-like wrinkles?
Many biologists favour the adaptationist approach to studying trait evolution. That is, they begin with ideas about why a certain trait might be adaptive and then proceed from there. Others (increasingly, myself included) may argue that there must be evidence that the trait is adaptive in the first place before such hypotheses are pursued. This may be a matter of preference or training or philosophical bent more than anything. However, it should be clear either way that there are good and bad ways to test adaptationist hypotheses.
Here’s the bad way:
Notice a trait and think up an adaptive function for it.
Assemble a small number of modern humans and get them to do whatever it is you think the trait is functional for (say, punching a heavy bag or picking up wet marbles). Make this unrealistic in terms of ancestral environments (e.g., use trained martial artists for punching or soak in 40°C water and handle glass marbles) and don’t control for other factors (say, warming up the hand).
Compare this as a binary trait rather than considering variation. For example, a buttressed fist vs. an open palm or fully wrinkled fingers vs. dry fingers.
Find a very weak effect, even with this extreme comparison.
Conclude that the trait in question evolved for the hypothesized function and ignore the obvious assumptions that are required for such a conclusion to hold.
Here’s a better way:
Notice a trait and determine the extent to which it varies within the study species.
Study the relationship between variation in the trait and performance of the proposed function. This would have been very easy for the marble study: soak hands for a few minutes to get partial wrinkles and assess performance, then soak for longer, etc. If this trait evolved as an adaptation, then differences in wrinkliness within the same finger should correlate with grippiness of that finger. (Here’s an example of that approach in studying the beaks of crossbills)
Explicitly address the necessary assumptions about ancestral traits, habitat, selective coefficients, and population size.
Use the comparative method within a phylogenetic context. Identify other species that have the trait and those that lack it. Has the trait evolved independently under similar conditions? Is it found in species that would not be expected to exhibit it if it evolves adaptively for a particular function?
Consider and rule out non-adaptive explanations (developmental constraints, pleiotropy, etc.) as much as possible.
Getting the data for this second list is much more difficult than for the first, but without them any conclusions about adaptive evolutionary history remain subject to the criticisms laid out several decades ago by Gould and Lewontin (1979).
Cales, L., R.A. Weber, and T.X. Temple (1997). Effects of water temperature on skin wrinkling. J. Hand Surg. 22A: 747-749.
Changizi, M., R. Weber, R. Kotecha, and J. Palazzo (2011). Are wet-induced wrinkled fingers primate rain treads? Brain Behav. Evol. 77: 286-290.
Gould, S.J. and R.C. Lewontin (1979). The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme. Proc. R. Soc. Lond. B 205: 581-598.
Kamran, H., L. Salciccioli, and J.M. Lazar (2011). Reduced water induced skin wrinkling in congestive heart failure. Clin. Auton. Res. 21: 361-362.
Kareklas, K., D. Nettle, and T.V. Smulders (2013). Water-induced finger wrinkles improve handling of wet objects. Biol. Lett., in press.
Reh, H. (1984). On the early postmortal course of “washerwoman’s skin” at the fingertips [in German]. Z. Rechtsmed. 92: 183-188.
Tsai, N. and S. Kirkham (2005). Fingertip skin wrinkling — the effect of varying tonicity. J. Hand Surg. 30B: 273-275.
Van Barneveld, S., J. van der Palen, and M.J.A.M. van Putten (2010). Evaluation of the finger wrinkling test: a pilot study. Clin. Auton. Res. 20: 249-253.
Weber, W. and R. Laufkötter (1984). Stage classification of washerwoman’s hands at experimental time intervals [in German]. Z. Rechtsmed. 92: 277-290.
Wilder-Smith, E.P.V. and A. Chow (2003a). Water-immersion wrinkling is due to vasoconstriction. Muscle Nerve 27: 307-311.
Wilder-Smith, E. and A. Chow (2003b). Water immersion and EMLA cause similar digit skin wrinkling and vasoconstriction. Microvascular Res. 66: 68-72.
Wilder-Smith, E.P.V. (2004). Water immersion wrinkling: Physiology and use as an indicator of sympathetic function. Clin. Auton. Res. 14: 125-131.
Win, S., L. Salciccioli, H. Kamran, P. Baweja, M. Stewart, and J.M. Lazar (2010). Water immersion-induced skin wrinkling is related to heart rate variability. Cardiology 116: 247-250.
A newer study does not support the original gripping results.
“It is demonstrable,” said he, “that things cannot be otherwise than as they are; for as all things have been created for some end, they must necessarily be created for the best end. Observe, for instance, the nose is formed for spectacles, therefore we wear spectacles. The legs are visibly designed for stockings, accordingly we wear stockings.”
– Candide by Voltaire
Humans are unique among the great apes (of which we are one) in various ways. One of them is our possession of a very long Achilles tendon, which is quite short in chimpanzees, gorillas, and orangutans.
Most anthropologists will tell you that this likely evolved as an adaptation for upright running, since it provides a great deal of spring in the stride. Or perhaps it’s just an inevitable byproduct of lengthening the lower leg. Yeah, sure, there’s evidence to support these hypotheses and everything. But I have another idea: I think the Achilles tendon evolved for dancing.
Think about it. Every human culture has some form of complex dance, but other apes don’t. And humans use dance as a way of attracting mates, displaying physical prowess, strengthening group bonds, and so on. So, we can imagine an advantage among our ancestors in being able to dance.
My evidence for this claim is not just the observation that other apes don’t dance and don’t have a long Achilles tendon, but also some direct measurements that I did. Specifically, I got 10 trained ballet dancers to do some pirouettes, and I measured how good their dancing was. Then I had them wear ski boots so that they couldn’t stretch their legs (thus simulating the short tendons of other great apes). And guess what? They couldn’t dance anywhere near as well.
Therefore, I conclude that dancing was a significant factor in the evolution of human leg anatomy. Sure, running might also be important, but dancing is a big part of the picture. Pretty compelling, eh?
Well, what if I did pretty much the same thing in order to claim that human hands evolving for making fists?
The derived proportions of the human hand may provide supportive buttressing that protects the hand from injury when striking with a fist. Flexion of digits 2–5 results in buttressing of the pads of the distal phalanges against the central palm and the palmar pads of the proximal phalanges. Additionally, adduction of the thenar eminence to abut the dorsal surface of the distal phalanges of digits 2 and 3 locks these digits into a solid configuration that may allow a transfer of energy through the thenar eminence to the wrist. To test the hypothesis of a performance advantage, we measured: (1) the forces and rate of change of acceleration (jerk) from maximum effort strikes of subjects striking with a fist and an open hand; (2) the static stiffness of the second metacarpo-phalangeal (MCP) joint in buttressed and unbuttressed fist postures; and (3) static force transfer from digits 2 and 3 to digit 1 also in buttressed and unbuttressed fist postures. We found that peak forces, force impulses and peak jerk did not differ between the closed fist and open palm strikes. However, the structure of the human fist provides buttressing that increases the stiffness of the second MCP joint by fourfold and, as a result of force transfer through the thenar eminence, more than doubles the ability of the proximal phalanges to transmit ‘punching’ force. Thus, the proportions of the human hand provide a performance advantage when striking with a fist. We propose that the derived proportions of hominin hands reflect, in part, sexual selection to improve fighting performance.
Put more simply, the authors did the following:
1) Observed that the proportions of the digits are different in human hands as compared to those of other apes. Specifically, “In comparison to other apes, humans have short palms and fingers (i.e. digits 2–5), but long, strong and mobile thumbs (i.e. digit 1)”.
2) Briefly discussed two main hypotheses that have been proposed to explain these hand proportions:
i) This is an adaptation for gripping. Specifically, this arrangement of digits allows two types of grip: one for precision and one for power. The long digits of other apes, by contrast, are adaptations for swinging and climbing (see, e.g., Tocheri et al. 2008; Almecija et al 2010).
ii) The short proportions of the fingers in humans are a byproduct of adaptive evolution of the feet, in which shorter toes evolved to facilitate upright walking. Because feet and hand development is regulated in similar ways developmentally, changing one has a secondary effect on the other (see Rolian et al. 2010).
3) Suggested a third hypothesis, namely that the proportions of our fingers evolved as an adaptation to making a well-supported fist, which allowed us (males, anyway) to punch each other with greater force and lower risk of injury.
4) Got 10 trained martial artists to hit a heavy bag equipped with accelerometers in order to measure the force delivered by forward, overhead, and sideways strikes using a fist versus an open palm. (For you karateka out there, this is a punch/tsuki, palm strike/teisho, and hammer fist/tetsui).
5) Measured the stresses exerted on parts of the hand in a fist or other striking positions.
6) Found that:
i) The fist delivers no more force than an open hand strike, but it does produce more “peak stress” on the target.
ii) A fist in which the fingers are curled in tight to the palm and the thumb is crossed over the fingers reduces the stresses on the hand and wrist relative to other hand positions.
7) Argued that a gripping hand could have evolved in several ways that would not have been compatible with a buttressed fist, and yet this is the hand shape that evolved.
8) Concluded that “the geometry of a fully buttressed fist provides a clear explanation for the specific skeletal proportions of the human hand”.
This is no different from the imaginary scenario about dancing and the Achilles tendon that I presented at the beginning. Both that imaginary study and this all-too-real one suffer from a number of serious flaws in both methods and logic. Let me outline just a few.
1) Assumptions about ancestral populations. If you want to claim that our hand proportions evolved as an adaptation (i.e., by natural selection) for pugilistic functions, then you need to postulate several things. One, that there was heritable variation in this trait among individuals in the ancestral population. Two, that individuals with slightly shorter fingers than those with slightly longer fingers made better fists OR that the change in finger length happened all at once in some mutant individuals. Three, that this ability to make better fists was actually important in affecting reproductive success. And finally, that this selective pressure was strong enough and sustained enough to result in the evolution of specific hand proportions over many generations. Obviously, the authors present absolutely no evidence to address any of these major assumptions. (At the very least, they could have quantified the extent of variation in human finger lengths among living individuals and correlated this with fist-making capability).
2) Unrepresentative sampling. Accepting for the sake of argument that 10 individuals is a sufficient sample size for a biomechanics study, there remains a major issue: namely, that most people don’t naturally punch with a properly buttressed fist. In fact, one of the first things that martial arts students need to be taught is how to make a fist. This study used trained martial artists, not people who punch using instinctual or intuitive hand positions. Indeed, the very fact that people need to be taught how to make a fist speaks against fist-making being a driving force in human hand evolution. If it were, there would also have to be a corresponding behavioural adaptation to actually make such a fist when hitting opponents.
3) Risk of injury remains high even with a buttressed fist. One of the reasons that martial artists practice open-handed strikes is that they are less likely to injure themselves when connecting with a solid target. Indeed, there are some punching-related injuries that are so common that they are called “boxer’s fracture” (fracture at the neck of the 4th or 5th metacarpal) and “boxer’s knuckle” (sagittal band tear). (I have suffered both, and they suck). To my knowledge, there is no “slapper’s fracture”.
4) Confusion of function and effect. Given its proportions, the human hand is capable of forming into a strong fist. It can also be used to play piano or type on a keyboard. We can also use it to shake hands or give each other the finger. It can throw and catch a ball. It can even be used to accentuate or replace spoken language. None of these is likely to have been a significant factor in shaping the evolution of the hand. Rather, these are functions that have arisen after the evolution of the hand’s current anatomy. This is a common theme in evolution. Structures evolve for one reason (adaptive or not), and then are co-opted into new functions. The results of this study are equally compatible with the notion that the human hand evolved its current proportions for some other reason, and then people figured out the best way to hit things with it. In fact, this strikes me as a much more plausible interpretation of the observations.
5) What about women? The hypothesis put forward in this paper is that sexual selection in the form of male-male combat contributed to the evolution of the human hand’s unique properties. Why, then, do women also have very similar finger proportions? One possible explanation is that hand development is rather constrained, so that adaptive changes in the hands of males carried over to changes in female hands as well. This is not unlike the best current explanation for why men have nipples: men have nipples because women need them, and they arise very early in development before sex-specific differences appear. But highly constrained hand development is a problem for the notion that hands evolved gradually for fighting.
6) Insufficient consideration of alternative (and much more plausible) hypotheses. As I noted previously, one of the major hypotheses for the evolution of human hand proportions is that it is a byproduct of the evolution of foot morphology for bipedal locomotion. Or the human hand could have been shaped directly by natural selection for gripping and tool use. Or some combination of these — perhaps developmental correlations with foot evolution gave the hand its general proportions, which were then refined by selection for specific functions. It seems obvious that tool use played an important role and that this would have exerted significant selective pressures in ancestral hominins. It would also be fully compatible with the fact that both males and females have the shortened hand proportions that we observe. Although the authors of the paper do mention these hypotheses, they do little more than pay them lip service. However, the fighting fist hypothesis adds no additional explanatory power.
To sum up, this is a paper that presents a small dataset of biomechanical analyses. It used an inappropriate sampling of subjects, and the only conclusions that can be drawn from the data are that the fists of trained martial artists are buttressed better than other arrangements of the hand. There is absolutely no information that is relevant to the question of why the human hand evolved as it did. (Note that this was not published in an anthropology or evolutionary biology journal). Moreover, to connect these observations with the evolutionary origin of human hand morphology requires some very unrealistic assumptions and a rather poor grasp of how one actually studies trait evolution.
The most impressive thing about this study is that it managed to gain so much attention with so little substance.