I recently received an email from a cognitive psychologist asking whether it is plausible that human use of language for deception is an adaptation. In other words, has there been sufficient time since humans began to speak for genetic variants associated with lying to rise to high frequency as a result of natural selection?
Here is my answer:
Last time I checked, expert opinion on when language evolved ranged from 2 million years ago to 40,000 years ago. The older number seems more plausible to me, but even if we take the most recent estimate that’s still at least 1,600 generations ago.
Imagine a gene with two alleles: t (for truth-teller) and l (for liar). Individuals with genotype tt always tell the truth. Individuals with genotype tl sometimes lie when it suits their interests—and have 1% higher reproductive success. Individuals with genotype ll always lie when it suits their interests and have 2% higher reproductive success. If the initial frequency of allele l is 0.0001, then after 1,600 generations it will be very nearly 0.999.
My model is obviously a gross over-simplification of how genetic variation might influence propensity to lie to get what you want. It is also a gross over-simplification of the mechanism of evolution in real populations. Among other things, I assumed an infinitely large population in which individuals chose their mates at random. But the model demonstrates the theoretical plausibility that genetic variation for verbal deception could lead to substantial evolution in the time we humans have been talking to each other.
You can try out other scenarios (stronger selection, finite populations, etc.) by playing with my AlleleA1 application. You will be able to do similar virtual experiments with the forthcoming Mendelian Pigs laboratory from SimBio.
Over the last several decades, population geneticists have published numerous empirical studies documenting rapid evolution in laboratory populations of insects. In my favorite recent example, researchers in Bruce Hay’s lab designed a new gene, inserted it into the chromosomes of fruit flies, established a lab population in which the novel gene was present at a known frequency, and watched the population evolve over 20 generations. Using a simple model like the one I used above, which assumes infinite population size, random mating, etc., they predicted that the allele’s frequency would rise from 0.25 to 0.90. Despite the model’s simplifications, the prediction was spot on.
Similarly rapid evolution has been seen in many natural populations. My favorite home-town example, featured in SimBiotic’s Evolution for Ecology SimUText chapter, comes from Katie Peichel’s lab at The Fred Hutchinson Cancer Research Center in Seattle. Peichel and colleagues documented change in the threespine stickleback population in Lake Washington following the cleanup of the lake in the 1960s. Before the cleanup, the vast majority of the sticklebacks had light armor plating (the extent of which is largely determined by a single gene with two alleles). By 2005, most of the fish had heavy armor plating.
As for documented examples of rapid evolution in human populations, an analysis of the S allele for beta hemoglobin—the allele associated with sickle-cell anemia—was published by Allison in 1965. Allison’s Table 4 shows the frequency of beta hemoglobin genotypes among Caribbean populations of African descent whose ancestors were forcibly relocated during the trans-Atlantic slave trade. Some of the present-day populations live on islands where malaria is common; others live on islands where malaria is rare. The frequency of the S allele is lower in the populations where malaria is absent. And it’s about what we’d predict using a simple population genetic model incorporating reasonable estimates for the frequency of the allele in the ancestral population, the fitnesses of the three genotypes in the absence of malaria, and number of generations that have elapsed since the forced founding of the new populations. (Students can explore the sickle cell example in SimBiotic’s Sickle-Cell Alleles lab.)
Another example is the evolution of life-long lactase production in human populations with a long history of dairying and drinking fresh milk. Other mammals, and most humans, stop making the enzyme after the age of weaning. This was undoubtedly the ancestral condition for us. Since the advent of dairying several thousand years ago, however, an allele of the lactase gene associated with adult lactase persistence has risen to a frequency of nearly 100% in some populations. Recent evidence indicates that this has happened more than once independently.
A third example: Human populations with a long history of eating a high-starch diet have more copies of the gene for amylase. This difference likely evolved, like lactase persistence, since the advent of farming.
All three human examples involve substantial evolutionary change in considerably less time than even the most recent estimates for when language evolved.
Finally, it seems worth noting that our capacity for deception likely predates our capacity for speech by tens of millions of years—if not hundreds of millions. Deception is widespread in nature. There are, to pick just a few examples, orchids that lie to their pollinators, flies that lie to their predators, and countless predators that lie to their prey. An entertaining (and fairly horrifying) case of auditory deception described was published in PLoS One last year.
Deception of conspecifics is common in primates, and correlates evolutionarily with brain size. The implication is that our ancestors were quite accomplished at lying to get what they want long before spoken language evolved. It seems likely that among the benefits that made speech advantageous was its utility as a tool for deception. And there’s been plenty of time since then for evolution by natural selection to refine this particular strategy.
Noble and Davidson argue for a recent origin of language in Noble, W., and I. Davidson. 1991. The evolutionary emergence of modern human behavior: Language and its archaeology. Man 26: 223-253.
Tobias argues for an early origin of language in Tobias, P. V. 1987. The brain of Homo habilis: A new level of organization in cerebral evolution. Journal of Human Evolution 16: 741-761.
The study on fruit flies from Bruce Hay’s lab is Chen et al. 2007. A Synthetic Maternal-Effect Selfish Genetic Element Drives Population Replacement in Drosophila. Science 316: 597–600.
The study on sticklebacks from Katie Peichel’s lab is Kitano et al. 2008. Reverse evolution of armor plates in the threespine stickleback. Current Biology 18: 769–774.
Allison’s analysis of sickle-cell anemia in the Caribbean is Allison, A. C. 1965. Polymorphism and natural selection in human populations. Cold Spring Harbor Symposium in Quantitative Biology 29: 137-149.
For a start on the literature on the evolution of adult lactase persistence, see Enattah et al. 2007. Evidence of still-ongoing convergence evolution of the lactase persistence T-13910 alleles in humans. American Journal of Human Genetics 81: 615–625 and Enattah et al. 2008. Independent introduction of two lactase-persistence alleles into human populations reflects different history of adaptation to milk culture. American Journal of Human Genetics 82: 57–72.
Documentation of differences among populations in copy number for the amylase gene is in Perry et al. 2007. Diet and the evolution of human amylase gene copy number variation. Nature Genetics 39: 1256–1260.
The story of auditory deception from PLoS One is Marshall, D. C. and K. B. R. Hill. 2009. Versatile Aggressive Mimicry of Cicadas by an Australian Predatory Katydid. PLoS ONE 4: e4185.
For the correlation between deception and brian size in primates see Byrne, R. W. and N. Corp. 2004. Neocortex size predicts deception rate in primates. Proceedings of the Royal Society B 271: 1693–1699.