Phenotypic red herrings, natural selection and the biological bases of behaviour: a cautionary cry.

•August 5, 2011 • 2 Comments

I have spent much of this week reading about the various schools of thought that have appeared, grown, merged or divided over the last sixty or seventy years on the topic of the biological or genetic bases or, put more succinctly, components of behaviour. After sorting through the important, and I must say from my own point of view admirable (in some places more than others of course), work of people like Lorenz, Tinbergen, Wilson, Hamilton, Maynard-Smith, Dawkins, the list goes on, and importantly those that opposed their work, a few consistent areas of concern became readily apparent to me. Some on the side of the ‘sociobiologists’ (an out of fashion term that I feel fits nicely in the modern context never the less) and others on the side of those that criticise their work as reductionist or misanthropic when applied to humans (social scientists and the like).

The general issue is as follows. I will explain how it affects both sides of this argument shortly.

As a post-graduate in the field of biological anthropology with a firm background in biology, and as a consequence the rudiments of genetics, I’m acutely aware of pleiotropy, epistasis, allometry and other factors that can see a given gene influencing multiple phenotypic traits, genes influencing one another and morphological traits affecting each other out of mechanical necessity. In short, I’m cautious about viewing a given trait (physical or behavioural should someone believe it to have some non-environmental basis) and exclaiming ‘this trait was selected for by natural selection and must therefore have a survival function’, this survival function fallacy births innumerable evolutionary scenarios that are likely to be absolute garbage. When wrangling with evolutionary ideas for a given organism I find it useful to have one of two approaches.

1) This is the most desirable approach though it is very rarely practical. Work from the genes up. Gene x produces protein y that influences cells of type a, b and c and thus tissue type z and so on and so forth. From this perspective one can see where the genetic influence begins to wane and the environmental factors begin to have more influence. Think of a connective tissue disorder as a convenient example, like Marfan syndrome, where a problem gene causes defective fibrillin produciton. This single gene, coding for a single protein, has multiple phenotypic effects that are then acted upon by the environment. I stress here that this same principle applies to genetic influencers of behaviour, a gene relating to a neural structure that has survival benefits would also drag with it numerous other effects that can be neutral or even slightly negative providing the cost doesn’t outweigh the benefit. Taking a magnifying glass to one of the incidental traits (what Gould would have called a ‘spandrel’) and looking for an evolutionary scenario that fits its selection is participating in the survival function fallacy.

2) Don’t start with the organism, start with the environment. If you cannot work from the genes up, work from the ecosystem down. Before conjuring evolutionary explanations for traits in a given organism, first make sure its environment is understood. This may help to sort important traits from those that are simply coincidental (pleiotropic perhaps etc.). Choose virtually any book on human evolution and you will see the consequences of starting the analysis with the organism. Scientists who start with any given hominin’s remains and then try to impose environments onto these remains will have a hard time sorting the wheat from the chaff, often with laughable results that damage reputations and waste the time of researchers and readers alike.

Gould & Lewontin summed up the perils of an ‘adaptionist’ approach very nicely in their 1979 paper ‘The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme’.

So, how does all of this relate to the work of those looking for the biological or genetic bases of behaviour? Put simply, are we really sure that any given behavioural pattern or what the ethologists would have called ‘instinct’ (convenient language, this is an outmoded notion) HAS a survival function? Was it simply pulled along with something that did? Is it a spandrel? This is perhaps my greatest criticism of a field of work that I do, otherwise, have great faith in. Workers in modern sociobiology and its offspring could perhaps benefit from working from one of the two approaches I outlined above.

As for the opponents of sociobiology of any modern type under whatever monicker it now takes (behavioural ecology, evolutionary psychology, gene-culture co-evolution etc.), I find a slightly different criticism for their approach which also relates to an understanding of genetics. Firstly, as any good geneticist or biologist of current times will stress, no modern day researcher in these fields truly believes in the false dichotomy of nature or nature. It is agreed upon that there are biological components and environmental components, the question is a matter of scale. Secondly, something I see time and time again in the criticisms of biological approaches to understanding behaviour is this old chestnut ‘the gene to phenotype to selection model of natural selection when applied to behaviour ignores choice, culture and other human attributes’. As mentioned above, this view of genetics is at its most innocent a gross simplification and at its worst absolutely erroneous. Unfortunately it is also widespread on both sides of the fence. Being erroneous, it is of course, not the basis of a good argument for or against anything. I also will reiterate here that no good biologist or biological anthropologist denies the role of culture and choice in shaping human beings, even with the numerous models for the survival function of culture and ideas about comparative cognition. Suffice it to say, meme models and comparative cognitive studies, if carried our responsibly, do not have to damage our concept of free will or our pride as a species.

Time will tell how things progress in this field, and I will be watching closely. I will provide a further exploration of this idea next week with an example from real world research, the work of Belyaev on the domestication of silver foxes.


House-husbands. Not so progressive after all…

•June 2, 2011 • 2 Comments

A terrific paper in Nature this month used an ingenious combination of strontium isotope analysis of molars from individuals of the species Australopithecus africanus and Paranthropus robustus and comparisons of molar size as indicators of sex (much greater sexual dimorphism in these early hominins) to come to two very interesting conclusions.

1) It would appear that in our early bipedal ancestors, and indeed cousins in the case of P. robustus,  it was more common for females to disperse from their place of birth and ally themselves with other ‘troops’ (for want of a better word) than it was for males. Males it would seem, enjoyed something of a ‘stay at home father’ lifestyle and had only relatively small ranges. This is in agreeance with what is seen in many modern human societies and those of our close extant relatives like the chimpanzees and bonobos (but not gorillas or other primates).

2) With the above point in mind, this challenges the notion that bipedalism evolved as a consequence of an increased need to move long distances, the so-called ‘endurance’ theories. Given my personal leanings toward the wading model put forward by Niemitz in Naturwissenschaften in 2007 and general unease with the unconvincing evidence for the endurance models I found these findings in Nature both exciting and in the best possible sense unsurprising.

There are of course other interpretations that are possible, such as the small home range being an example of a preferred habitat (cave-dwelling). If this were the case the species in question may roam further under more general circumstances but I find that unlikely. I anticipate that future evidence will support the ‘small range’ idea above as a general behavioural truth about our ancestors.


“Strontium isotope evidence for landscape use by early hominins”

Copeland, S., Sponheimer, M., Ruiter, D., Lee-Thorp, J., Codron, D., Roux, P., Grimes, V. & Richards, M.

NatureVolume: 474, Pages:76–78 Date published:(02 June 2011)

Neanderthals were right handed… Should we be surprised?

•May 23, 2011 • 2 Comments

An article in science news this week puts forward the argument for population level Neanderthal right handedness based on stone tool scratch patterns on the front teeth of 500,000 and 30,000 year old Neanderthal remains. It’s a nice find but shouldn’t be all that surprising given the findings about ape handedness published earlier this month (see one of my earlier posts: If all extant African apes display population level right handedness (us included of course) then it is no surprise at all that one of our closest extinct cousins would as well. I don’t think I’m going out on much of a limb to suspect that the shared common ancestor of all extant African apes had at least a tendency toward right handedness, in fact this is what was implied in my previous post on the matter.

Hoffecker, the ‘super-brain’ and genetic similarity.

•May 19, 2011 • 4 Comments

Today I came across a summary of a conversation with John Hoffecker, an American paleoanthropologist of the University of Colorado Boulder, about the relationship between the cultural explosion seen in human artifacts, especially art works, beginning at least 75,000 years ago and the evolution of the ‘modern human mind’. In the context of this particular piece, ‘human mind’ refers to our capacity to communicate abstract and novel ideas through speech or symbolism, not of course the brain, the physical size and structure of which had already been changing for a long time prior to the appearance of modern man.  This got me thinking about the idea put forward by Flannery in ‘Here on Earth’ that it may have been a reduction in genetic diversity in early H. sapiens that led to elevated levels of cooperation and altruism (much the same way as it does in ants or bees due to close genetic relationships). I wonder if a significant genetic bottleneck occurred at about the same time as this abstract cultural revolution? Could increasing cooperation and altruism have led to a greater capacity, or perhaps put more succinctly, need, to share thoughts?  I’m going to have a look at the literature and see what I come up with. I’d welcome the suggestion of any articles from readers that may broach this topic. Beware however that many articles in this area are filled with teology and science ruining anthropocentrism, so keep your Ockham’s razor and objective mindset at the ready.

Exciting stuff. It was after all, most likely this cultural paradigm shift (genetic in nature or otherwise) that led to agriculture, civilisation, government and technology advances like desktop computers and electric tea-kettles. Well worth the effort of investigation.

UPDATE: It just so happens that prevailing thought is that a bottleneck/s of some kind occurred around the 70,000 ya mark or more recently. Parsimony at work! I found the following papers relating to this;

You can find the summary of the chat with Hoffecker here:

Nut-cracker man no more!

•May 17, 2011 • 3 Comments

A curious paper found its way out from my “to read” pile today and to be honest I’m sad I hadn’t looked at it sooner. Paranthropus boisei is not my favourite hominid, so I shuffled this particular piece to the bottom of my priority list, shame on me. The paper titled “Diet of Paranthropus boisei in the early Pleistocene of East Africa” (not too interesting a title, perhaps why I neglected it) turned out to be something of a shocker. The last time I encountered P. boisei was in an undergraduate evolution unit where we briefly discussed its impressive dentition and prominent sagittal crest as adaptations to eating nuts. Guess we can be rid of that particular notion.

This study used isotope analysis to demonstrate that the staple of the P. boisei diet was neither nuts nor the other C3 staples of known primates like fruit or leaves but the much less nutritious C4 plant types; grasses or sedges. This is quite a find. It demonstrates that at least some ancient bipedal hominids occupied an econiche entirely different to what the last 50 years of anthropological thought would suggest. This means that P. boisei would have been competing for resources with other grazers like zebra ancestors or hippos, quite an unexpected evolutionary scenario. As for those large, flat teeth, it would seem they were used less for bite force and more for the continuous processing of large quantities of low quality fodder. I wonder what this means for robustus? Guess I’ll have to look into that.

Paranthropus boisei: would have enjoyed being your lawnmower.


“Diet of Paranthropus boisei in the early Pleistocene of East Africa”

Thure E. Cerling, Emma Mbua, Francis M. Kirera, Fredrick Kyalo Manthi, Frederick E. Grine, Meave G. Leakey, Matt Sponheimer & Kevin T. Uno.

Proceedings of the National Academy of Sciences, May, 2011

Last of the Neanderthals?

•May 13, 2011 • Leave a Comment

I’m in the middle of writing a paper at the moment so I won’t describe this article at length here. Briefly, this fascinating piece in ABC Science suggests that the (or at least one of the) last refuges of the Neanderthal may have been discovered. I will tentatively add something here; given the recent discovery of Denisova in a relatively proximal part of the world, how sure are we that these tools were made by what we would traditionally call Neanderthal?

Ancient urbanization and tuberculosis resistance.

•May 10, 2011 • 5 Comments

Tuberculosis is a bit of a pet topic of mine, so this article from the March 2011 edition of Evolution caught my eye:

“Ancient urbanization predicts genetic resistance to tuberculosis.”

Barnes, I., Duda A., Pybus, O. & Thomas, M.

It is logical that an increase in urbanization and consequent close quarters association between large numbers of people would increase both the incidence and prevalence of various transmissible diseases. As described by Diamond in “Guns, Germs & Steel”, this leads to the tendency of a given urbanized population to develop greater rates of resistance to the pathogens responsible for these disease states. The article above explores this assumption by measuring the frequency of an allele (SLC11A1 1729 + 55del4) related to resistance to infection by Mycobacterium tuberculosis, the aetiological agent of tuberculosis, against the estimated length of time a given population has been urbanized. In reinforcing my initial statement, the results showed a strong positive correlation between how long ago a population shifted toward urban living and rates of this TB resistance related allele. So, as would be expected, more ancient population centres in the middle east for example showed relatively high frequencies of this allele when compared to southern African or Scandinavian populations.

The correlation between resistance related alleles and urbanization could be used for other, more novel, studies. For example, frequency testing for this allele or others associated with resistance to diseases endemic to urban centres, could be used in something of a ‘forensic’ manner to detect descendants of population centres that have undergone collapse i.e. the now dispersed members of ancient African or Mesoamerican populations.

On a side note; I found it a little unusual that this study also measured TB resistance against the time at which cattle were domesticated. As mentioned in a previous post ( it is highly unlikely that humans acquired this infection from cattle, the chromosomal data just doesn’t make sense in that context. Nor does the presence of TB in the New World make sense if cattle were the vector. With these things in mind I really hope they were simply speaking of M. bovis infection (as opposed to M. tuberculosis infection) only in terms of how it could produce a similar selection pressure for the given resistance allele. Even in this case I hypothesise that the role of M. bovis would relatively minor. Hopefully this particular myth of tuberculosis (of the human strain) as a zoonosis of bovine origins will someday find its rightful place in the dustbin.