Published on:

By Simon Fisher and Matt Ridley

Simon Fisher and I have published a Perspectives article in
Science magazine.


From Science magazine:

by Simon E. Fisher and Matt Ridley

(Simon E. Fisher, Department of Language and Genetics, Max
Planck Insti- tute for Psycholinguistics, Nijmegen 6525 XD,
Netherlands. 2Donders Institute for Brain, Cognition and Behaviour,
Radboud University, Nijmegen 6525 EN, Netherlands. Matt Ridley,
House of Lords, London SW1A 0PW, UK. E-mail:

State-of-the-art DNA sequencing is providing
ever more detailed insights into the genomes of humans, extant
apes, and even extinct hominins
13), offering
unprecedented opportunities to uncover the molecular variants that
make us human. A common assumption is that the emergence of
behaviorally modern humans after 200,000 years ago required—and
followed—a specific biological change triggered by one or more
genetic mutations. For example, Klein has argued that the dawn of
human culture stemmed from a single genetic change that “fostered
the uniquely modern ability to adapt to a remarkable range of
natural and social circumstance” (
4). But
are evolutionary changes in our genome a cause or a consequence of
cultural innovation (see the figure)?

Many nuanced accounts of human evolution implicitly assume
that biological changes must precede cultural changes.
et al. described how
alterations in size, wiring, and physiology of the human brain
yielded advanced cognition, and hence a transformation of
behavioral repertoires that encompassed everything from language
and tool use to science and art. They posited that it is because of
complex cognition that human beings are uniquely capable of
cultural evolution, rather than vice versa
5). In a recent paper that elegantly
emphasizes the importance of gene expression and metabolic changes
in human evolution, Somel
et al. adopt a
similar view. They argue that a small number of mutations, altering
the structure or expression of developmental regulators, drove the
emergence of human cognitive traits to trigger a cultural explosion
around 200,000 years ago (

This prevailing logic in the field may put the cart before
the horse. The discovery of any genetic mutation that coincided
with the “human revolution” (
6) must take
care to distinguish cause from effect. Supposedly momentous changes
in our genome may sometimes be a consequence of cultural

innovation. They may be products of culture-driven gene evolution

In certain cases this is obvious. Lactase-persistence mutations
did not trigger dairy farming; they spread as an evolutionary
response to dairy consumption (8). The higher alcohol tolerance of
Europeans relative to Asians did not prompt, but followed, greater
alcohol consumption in Europe (9).

Such examples are mostly drawn from after the Neolithic
revolution and the invention of agriculture. But culture-driven
gene evolution may have also operated earlier in human history and
could be key to understanding our origins. Wrangham’s argument (10)
that the invention of fire and cooking altered human gut size 2
million years ago is a case in point, positing that genetic change
was contingent on prior cultural innovation.

Under the culture-driven view, many critical genomic alterations
that facilitated spoken language, for example, might have spread
through our ancestors after this trait emerged.

That is, prior behavioral changes of the species provide a
permissive environment in which the function- ally relevant genomic
changes accumulate. The selective advantage of a genetic change
that increased language proficiency would likely be greatest in a
population that was already using language.

Take the FOXP2 gene. More than a decade ago, rare FOXP2
mutations were implicated in an unusual inherited disorder:
Affected people have problems coordinating sequences of mouth
movements that underlie fluent speech, accompanied by difficulties
in expressing and under- standing language (11). Sequencing of
versions of FOXP2 in other primates revealed that two evolutionary
changes in the protein-coding part of the gene occurred in the
human lineage after it split from that of the chimpanzees (12).
There was also evidence of recent Darwinian selection acting at the
locus (12). The findings prompted speculation that alteration of
FOXP2 triggered the explosion of creativity marking the
emergence of behaviorally modern humans (4). Further studies have
suggested that the changes to the human FOXP2 protein pre- dated
the splitting of Neandertals and mod- ern humans several hundred
thousand years ago (13). Most recently, researchers have pin-
pointed intronic noncoding changes at the FOXP2 locus that arose
after the split from Neandertals and that might have affected how
the gene is regulated (2).

In considering the roles of FOXP2 in human evolution, it is
important to recognize that it has a deep evolutionary history.
Animal studies indicate ancient conserved roles of this gene in
patterning and plasticity of neural circuits, including those
involved in integrating incoming sensory information with outgoing
motor behaviors (14). The gene has been linked to acquisition of
motor skills in mice and to auditory-guided learning of vocal
repertoires in songbirds (14, 15). Contributions of FOXP2 to human
spoken language must have built on such ancestral functions.

Indeed, further data from mouse models suggest that humanization
of the FOXP2 protein may have altered the properties of some of the
circuits in which it is expressed, perhaps those closely tied to
movement sequencing and/or vocal learning (13).

Given these findings, it seems unlikely that FOXP2 triggered the
appearance of spo- ken language in a nonspeaking ancestor. It is
more plausible that altered versions of this gene were able to
spread through the populations in which they arose because the
species was already using a communication system requiring high
fidelity and high variety. If, for instance, humanized FOXP2
confers more sophisticated control of vocal sequences, this would
most benefit an animal already capable of speech. Alternatively,
the spread of the relevant changes may have had nothing to do with
emergence of spoken language, but may have conferred selective
advantages in another domain.

FOXP2 is not the only gene associated with the human revolution
(3). However, it illustrates that when an evolutionary mutation is
identified as crucial to the human capacity for cumulative culture,
this might be a consequence rather than a cause of cultural change
(8). The smallest, most trivial new habit adopted by a hominid
species could— if advantageous—have led to selection of genomic
variations that sharpened that habit, be it cultural exchange,
creativity, technological virtuosity, or heightened empathy.

This viewpoint is in line with recent understanding of the human
revolution as a gradual but accelerating process, in which features
of behaviorally modern human beings came together piecemeal in
Africa over many tens of thousands of years (6). Recognizing the
role of culture-driven gene evolution in the origins of modern
humans provides a powerful reminder of how easy it is to confuse
cause and effect in science.


References and Notes

1. M. Meyer et al., Science 338, 222 (2012).

2. T. Maricic et al., Mol. Biol. Evol. 30, 844 (2013).

3. M. Somel, X. Liu, P. Khaitovich, Nat. Rev. Neurosci.
14, 112 (2013).

4. R. G. Klein, The Dawn of Human Culture (Wiley, New York,

5. E. J. Vallender et al., Trends Neurosci. 31, 637 (2008). 6.
S. McBrearty, in Rethinking the Human Revolution, P. Mellars,
K. Boyle, O. Bar-Yosef, C. Stringer, Eds. (McDonald Institute for
Archaeological Research, Cambridge, UK, 2007), pp. 133–151.

7. P. J. Richerson, R. Boyd, Not by Genes Alone (Univ. of
Chicago Press, Chicago, 2004).

8. K. N. Laland et al., Nat. Rev. Genet. 11, 137 (2010). 9. J.
Diamond, Guns, Germs and Steel (Norton, New York, 1997).

10. R.Wrangham, Catching Fire:How Cooking Made Us Human
(Basic Books, New York, 2009).

11. C. S. Lai et al., Nature 413, 519 (2001).

12. W. Enard et al., Nature 418, 869 (2002).

13. W.Enard,Curr.Opin.Neurobiol.21,415(2011).

14. S. E. Fisher, C. Scharff, Trends Genet. 25, 166 (2009). 15.
C. A. French et al., Mol. Psychiatry 17, 1077 (2012).

Acknowledgments: S.E.F. is supported by the Max Planck Society.
We thank D. Dediu for helpful comments.


By Matt Ridley | Tagged:  rational-optimist