Nothing in Biology Makes Sense Except in the Light of Evolution, Theodosius Dobzhansky (1973). The American Biology Teacher, 35(3), 125-129.

“See the lilies of the field…their genomes are 36 times larger than ours…”

Those with a naïve understanding of evolution would have a difficult time understanding how a flowering plant could contain 36 times more DNA than humans. After all, DNA is the code of life.  DNA codes for proteins and thus one might think that more DNA would mean greater biochemical complexity.  Indeed, those who think of evolution as inexorably leading from simplicity to complexity would have a hard time fathoming how this could be true.  For example, it is true that prokaryotes have much less DNA than Eukaryotes.  The bacterium Escherichia coli contains 4.6 x 10⁶ base pairs (bp); whereas the fungus Nuerospora crassa has 3.99 x 10⁷ bp and animal Homo sapiens sapiens (humans) contain 5.93 x 10⁹ bp. However there is a greater than 200,000-fold genome size diversity in Eukaryotes and this variation has no relationship to organismal complexity¹. 

A decade ago this disparity was called the c-value paradox².  The c-value refers to the haploid genome size of an organism.  If the mean genome size of groups were plotted, it would occur in this order: bacteria (~10⁶ bp); algae and fungi (between 10⁷ to 10⁸ bp); worms (10⁸ bp); insects (10⁸ – 10⁹ bp); echinoderms (10⁹ – 10¹⁰ bp); fish (10⁹ – 10¹⁰ bp); reptiles (10⁹ – 10¹⁰ bp); birds (10⁹ – 10¹⁰ bp); mammals (10⁹-10¹⁰ bp); amphibians (10⁹ – 10¹¹ bp); flowering plants (10⁹-10¹⁰ bp.)  There is no clear or easy way to make sense of these numbers.  For example, this order doesn’t correlate with organismal complexity or even age in the fossil record³.  The genome sizes within more narrow groups defy easy explanation as well, for example the genus Pinus (pines) has a range from 1.8 x 10¹⁰ to 4.0 x 10¹⁰, which is generally larger than flowering plants⁴.  The flowering plant Arabidopsis thaliana has a tiny genome in comparison, only 1.57 x 10⁸.

What is really interesting however is what percentage of the DNA of Eukaryotes actually codes for proteins (or has a known function relating to the coding of proteins.) For example, in humans only 3% of the genome codes for proteins, and maybe another 10% have an identified role in regulating gene expression⁵.  In this sense, humans are typical and this means that at least 85% of eukaryotic DNA does not directly influence protein coding.  So what are the characteristics of this non-coding DNA?  How did it get there?  How is this non-coding DNA maintained through evolutionary time?  Is it really junk-DNA, as described by many early researchers?

The recent sequencing of a large number of eukaryotic genomes has provides a more accurate understanding of their DNA content and type. These are shown below:

Explaining the existence of structural genes is simple.  Clearly, all organisms require proteins to carry out the biochemical properties of life.  Some of these proteins must be produced in large amounts and so the existence of repetitive structural genes is also easy to explain.  How then do we explain the rest? This problem has been recently called the c-value enigma.

There are five main theories addressing this problem; junk-DNA, selfish-DNA, nucleoskeletal-DNA, nucleotypic-DNA, genome protection⁶.  The first two theories can be lumped together as mutation pressure theories and the last three are optimal DNA content theories.  The junk-DNA hypothesis says that the accumulation of genetic material in various organisms occurs by random process (genetic drift.)  If this hypothesis were true is would predict that there are no grand-level correlations between DNA content and organismal complexity. However, there do seem to be correlations between cell volume and genome size.  Junk-DNA would address this as a result, not a cause.  In other words, since there is more DNA, the cells of that particular organism must get larger.  It fails to adequately explain however the fact that there are some correlations between DNA content and life-history features within lineages, it assumes that cells cannot delete excess DNA, and there is no evidence of a steady accumulation of DNA content through evolutionary tine (which would be required by a drift mechanism.)

Originally, it was thought that the c-value paradox could easily be explained by selfish-DNA.  Selfish genetic elements can copy themselves and in theory have no impact on the host organism’s fitness so long as they replicate in non-coding regions of the genome.  Clearly, replication in the coding regions would result in massive mutation with major impacts on fitness.  Several human diseases result from transposable genetic elements replicating in a coding region.  For example, the alu elements are short interspersed elements (SINES) that have DNA recognition sequences that react to the restriction endonuclease AluI.  They are 200 – 300 base pairs long and can be present in the genome up to 900,000 times.  A common alu insertion occurs at the angiotensin converting enzyme (ACE) locus results in a polymorphism that affects the activity of this enzyme. The D-allele is characterized by an absence of these alu insertions, and thus has higher enzymatic activity than the I-allele which has the alu insertion. The frequency of the D and I alleles are similar in persons of African descent found in Nigeria, Jamaica, and the United States.  However individuals with the D-allele are more likely to develop hypertension only in the Western hemisphere (indicating gene x environment interaction.) Another 306bp Alu insertion polymorphism occurs in the progesterone receptor gene (PROGINS on chromosome 11) is associated with an increased risk of breast cancer. The insertion was found at a frequency of 5%, 10%, and 14.6% in East Indian women with endometriosis, uterine fibroids, and breast cancer.  The control group (women w/o these diseases) had a frequency of only 5.5% Thus, only the breast cancer group showed a statistically significant difference⁷.  The frequency of this insertion polymorphism differs widely in human populations:

European American, 0.208, N = 72

African American, 0.021, N = 71

Hispanic American, 0.164,  N = 76

Mvskoke (Creek), 0.041, N = 37

Pakistani, 0.09, N = 55

East Indian, 0.055, N = 490

From this we would include that all factors being equal, PROGINS associated breast-cancer should be 10 times more frequent in European American women as African American women. The fact that transposable genetic elements do cause disease indicates there should be serious selection for means to regulate their insertion sites away from exons.

Overall transposable genetic elements make up approximately 51.3% of the human genome (SINES 16.1%, LINES 22.3%, LTR retrotransposons 9.3%, DNA transposons 3.6%.) This figure varies widely across phylogenetic groups (F. assyrica, lilies 95-99%, Zea mays, corn 60%, A. thaliana, cruficer 14%, T. negroviridis, fish 0.14%, T. rubripes, fish 2%, R. esculenta, frog 77%, X. laevis, frog 37%, D. melanogaster, fruit fly 15-22%, A. gambiae mosquito 16%.)  Again the selfish-DNA hypothesis suffers from not explaining the existing correlations between DNA content and life-history features, assumes that cells cannot delete excess DNA or regulate transposition, and would require a steady accumulation of DNA content across evolutionary time.  For example, how does it explain the disparities in TGE content between fish, amphibians, and mammals (all of whom share a common ancestor?) 

The nucleoskeletal hypothesis suggests that the increased amounts of DNA in eukaryotic genomes are a mechanism by which their nuclear size is selected to meet the needs of the cell for balanced growth.  This idea is supported by the strong relationship between cellular DNA content and cell volume.  Gregory (2000) showed a highly significant correlation between these variables for erythrocytes in 159 species of vertebrates (jawless fishes, cartilaginous fishes, teleost fishes (excluding lungfishes), lungfishes, urodele amphibians, anuran amphibians, reptiles, and birds⁸. One mechanism accounting for this relationship is the idea that the transfer of messenger and ribosomal RNA from the nucleus to the cytoplasm via nuclear pores is a limiting factor on cell growth.  Thus we can imagine cases in which we have smaller cells, with smaller transfer rates, but quicker growth versus larger cells with larger pores and slower growth rates.  DNA amount in the cell is seen as a way of “providing space for the nucleus” which in turn impacts the size of its connections to the cellular transport membranes.  The problem with this hypothesis is that it doesn’t explain imperfect scaling between cell size and DNA content in some groups.  For example imperfect scaling occurs in lungfish and salamanders where cell volumes scales in a strongly positive allometric fashion with changes in genome size and there is a negative correlation between C-value between both cell division and developmental rates⁹.  One extreme example of this is the relationship between very large genome size and neoteny in salamanders.  Neoteny is when juvenile characters are retained in adults.  Neotenic salamanders have the largest genomes in amphibians (and as you already know amphibians have some of the large genomes of all organisms¹⁰.)  It also cannot explain instantaneous reductions of cell size that occur following reduction of DNA content, and is incompatible with observation of quantum genome size shifts (as happens with polyploidy.)

The nucleotypic hypothesis states that DNA content directly affects cell size and cell division rate. There is strong evidence that DNA content has a strong negative correlation with rates of both meiotic and mitotic cell division in a variety of organisms¹¹.  The mechanism of this relationship results from the notion that more DNA should cause a greater duration of the S-phase of the cell cycle (DNA replication.)  This results from there being an imperfect relationship between increased DNA content and replicon number amongst other mechanisms. In addition all aspects of the cell cycle are increased with greater DNA content. There is some variation in the nature of the relationship between mitotic rate and DNA content.  For example in dicots the cell cycle is longer per amount of DNA than it is in monocots (although the scaling is similar.)  The relationship between meiotic rates and DNA content is more complex.  Animals tend to have longer meiotic rates than plants per DNA content and within animals mammals have longer rates than amphibians or insects.  The main problem with the nucleotypic hypothesis is that there is not yet enough data to fully test it and no satisfactory mechanism has been proposed to explain why it works.

Finally, Patrushev and Minekevich propose a unique optimal model to explain excess DNA content¹².  Under normal cellular conditions, endogenous chemical mutagens cause spontaneous mutations.  In a variety of biochemical reactions reactive metabolites are formed as intermediate byproducts which can wreak havoc on DNA. In substrate redox reaction involving oxygen free radicals are always formed and in aerobic organisms 4-5% of molecular oxygen is transformed during respiration to reactive oxygen species (ROS.)  In a typical human cell this can mean as many as 50,000 – 200,000 mutations daily! These authors argue that one role of the non-coding DNA is to act as a sink to absorb ROS.  Thus, by chance alone in the human genome size at 3 x 10⁹, there is a ~97% chance that a ROS damage event occurs in a non-coding segment, and a 87% chance it occurs in a segment that does not impact coding or regulation of coding. If there was no non-coding DNA, than 100% of mutations would occur in regions that impact the organism’s fitness.  Thus, under this model, there would be positive selection for genomes to allow the increase of TGE’s within non-coding segments of the genome.  The fact that there are variations in genome sizes amongst Eukaryotes would be predicted, especially if any of the other mechanisms mentioned above were in action.

In conclusion, the c-value enigma is a scientific question that requires more attention.  Genome sizes are distributed in a non-random fashion, but at present we don’t have a unifying theory that can explain the variation.  Mutation pressure theories explain some issues but fail at others.  Optimal size evolution theories suffer from some of the same difficulties as all adaptive program hypotheses.  My intuition suggests that genome sizes result from compromises between mutational and optimal forces.  We may not ever be able to develop a general c-theory, leaving us with only specific mechanisms that account for variation within specific groups.  What we know about genome variation does accomplish is the demolition of progression theories of evolution.  Lily DNA results from evolutionary issues specific to flowering plants as human DNA content results from those experienced by mammals.

Notes

1. Gregory, T.R, Coincidence, coevolution, or causation?  DNA content, cell size, and the c-value enigma, Biol. Rev. 76: 65-101, 2001.
2. Klug, W and Cummings, R, Genetics 5th edition, (Upper Saddle River, NJ: Prentice Hall), 1997.
3.  Genome sizes are provided by Klug and Cummings, as well as from Bionumbers. 
4. Morse, A.M. et al, Evolution of genome size and complexity in Pinus, PLOS One 4(2): e4332, 2009.
5. Patrushev, L.I. and Minkevich, I.G, The problem of eukaryotic genome size, Biochemistry (Moscow) 73(13): 1519-1551, 2008.
6. Gregory T.R. 2001 and Patrushev, L.I. and Minkevich, I.G. 2008.
7. Govindan, S et al., Association of progesterone receptor gene polymorphism (PROGINS) with endometriosis, uterine fibroids and breast cancer, Cancer Biomark. 2007; 3(2):73-8.
8. Gregory, T.R., Nucleotypic effects without nuclei: genome size and erythrocyte size in mammals, Genome 43: 895-901, 2000.
9. Cavalier-Smith, T, Skeletal DNA and the evolution of genome size, Annual Rev. Biophysics and Bioengineering 11: 273-302 and Gregory, T.R., 2001.

10.  Cavalier-Smith, Coevolution of vertebrate genome and, cell, and nuclear sizes. In Selected Symposia and Monographs U.Z.I., vol. 4 (ed. G. Ghiara et al.), pp. 51-86.

11.  Gregory, T.R. 2001.

12.  Patrushev, L.I. and Minkevich, I.G, 2008.

Luke Skywalker, Han Solo, and the Importance of Adaptation Implementation in Evolutionary Psychology

I’m not going to lie. If you follow my work at all, hopefully this isn’t a surprise – I try to stay honest – it’s a way to compensate for my deficits. Lots of folks I know – several of whom I consider good friends – report that they just can’t stand evolutionary psychology. Some seem to think it’s the devil – morally and scientifically irresponsible and reprehensible. I do my best to deal with things, but every now and then, honestly, I just shake my head. And sometimes I just have to write about it.

A few weeks ago, a really interesting discussion about the mating-relevant differences between Luke Skywalker and Han Solo emerged in my graduate course in social psychology. This was one of these moments when a thread of the fabric of American culture and the content of the course interfaced perfectly.

Luke is prototyipically non-masculine – whiny and wimpy throughout three episodes. Han is just macho. He plays it cool, doesn’t need anyone’s help, and has classic masculine good looks.

What’s attractive about Luke? What’s attractive about Han? The conversation touched on several themes relevant to evolutionary psychology – mate choice, optimal features of long-term mates, optimal features of short-term mates, morphological features of sexually attractive males, the handicap principle applied to high levels of testosterone, inbreeding depression, and so forth. It was an exciting class discussion that put a face to many of the concepts from the readings of the week.

About a week later, I had a passing conversation with a long-time academic friend – who’s, notably, not a huge fan of evolutionary psychology. Somehow, I briefly mention this great class discussion – and my friend sort of scoffs – saying something like “can’t it be just that Han Solo would be way better in bed? It’s not like I’d want to have babies with him!”

I’ve learned to not bother arguing about evolutionary psychology in certain circles – but my mind immediately went to a conversation I’d had with David Schmitt when he visited New Paltz last year (to give a talk about mating psychology on Darwin’s 200th birthday). David is, of course, a leading thinker and researcher in the field – and the only thing as substantial as the academic rigor of his work is his reasonable take on things. An expert on the nature of psychological adaptations (see Schmitt & Pilcher, 2004), David introduced me to the distinction between “adaptation implementers” and “fitness optimizers” (a conception that he attributed to his mentor David Buss, a luminary in the field).

If we think of organisms as designed by evolutionary forces to propagate their own genes (Dawkins, 1976), we can have two general ways of understanding organisms. Perhaps (a) organisms are “fitness optimizers,” designed to consciously do whatever it takes to successfully produce viable progeny. On the other hand, perhaps organisms are “adaptation implementers,” designed with a battery of specific adaptations that, on average, had the effect of increasing the reproductive success of the organism’s ancestors compared with conspecifics without said adaptations.

OK – so let’s put a face to all this. Think about pregnancy sickness, famously studied by Margie Profet (1992). If pregnancy sickness is conceptualized from a fitness-optimization perspective, then pregnant women are essentially framed as conscious of the deleterious effects of certain foods on their babies, and they make themselves sick to certain stimuli as a result. If women with pregnancy sickness are, instead, framed as “adaptations implementers,” then the fact that they tend to get sick in certain contexts (e.g., when eating certain foods that are likely to possess toxins) is the result of this psychological and physiological tendency (that we call pregnancy sickness) to have increased the fitness of ancestral women – regardless of conscious thought surrounding the reproductive benefits of pregnancy sickness.

As Dave put it to me, evolutionary psychology sees humans as “adaptation implementers” – not “fitness optimizers.”

This important construct can be applied, really, to any adaptation. Think about fear of heights – one of the most basic and culturally universal fears. On one hand, we can think of this fear in terms of “conscious fitness optimization” – with people thinking “I know that if I fall 100 feet, that’s it for me – and my entire genetic lineage – ouch!” OR we can think of expressed fear of heights as explicating “adaptation implementation.” In this way, we can think of a natural fear of heights as the product nature selecting for ancestors across generations who happened to, by chance – and likely unconsciously – fear heights. In this way, someone expressing a fear of heights is simply implementing an adaptation that, on average, across generations, gave the ancestors of people with a fear of heights a reproductive advantage over others.

This same line of reasoning makes it so that modern-day contraception is not a deal killer for evolutionary psychology. I’ve heard people argue essentially that “well if evolutionary psychology says we do everything to propagate our genes, but we use contraception and many of us CHOOSE to not have kids, doesn’t that just say that evolutionary psychology is all wrong?” No. Actually. It doesn’t. Such an argument does, however, suggest that the conscious fitness-optimization approach to evolutionary psychology is completely misguided. If we were designed to consciously maximize fitness regardless of any other factors, then maybe contraception would not be as prevalent as it is – and maybe more people would choose to have children. But, in fact, people who use contraception (and there are lots of us out there) are still products of evolution whose psychologies are filled with adaptations. Contraception users still fear heights, spiders, and snakes more than other stimuli. Contraception users still show nepotistic tendencies when considering whom to help in emergency situations. They still get angry at being cheated by others in their close social circles. Contraception users experience the basic emotions of joy, sadness, surprise, disgust, and anger – and contraception users can identify these emotional states accurately in humans from across the globe. And they still find spoiled milk totally gross. Contraception users are attracted to the same features in mates that non-contraception users are attracted to – they still prefer that a mate be kind, intelligent, witty, and attractive. And, back on task, female contraception users still find Han Solo more sexually attractive than Luke Skywalker. That is, they implement psychological adaptations – regardless of conscious efforts to reduce the likelihood of reproducing. And this is exactly what we would expect in organisms that are designed to implement a battery of fitness-increasing adaptations – as opposed to organisms with general-purpose mechanisms designed to consciously increase reproductive success regardless of environmental conditions.

Being a person who uses contraception and chooses to not have children does NOT make that individual a person whose behavior and psychology are unrelated to the evolutionary history of homo sapiens

Back to the Order of the Jedi: Think about the sexual attraction that a heterosexual woman may feel toward Han over Luke. I haven’t done a poll, but suppose we find evidence that more heterosexual women find Han sexually attractive than Luke – thus, corresponding to a non-random mate-choice situation. Is it accurate and comprehensive to just say that Han would probably be better in bed? I don’t think so! I think that such a response actually screams for a distinction between fitness optimization and adaptation implementation!

In the domain of short-term mating, there are reasons underlying why women are attracted to masculine-looking men – with muscular bodies, high shoulder-to-hip ratios, deep voices, and symmetrical faces (Shoup & Gallup, 2008). And an evolutionary perspective on why women are attracted to such Han Soloesque features does not need to presume that women want to have Han’s baby! When we think of adaptation implementation, this way of thinking, in fact, can be greatly elucidated. It’s not enough to say that a woman would rather sleep with Han than Luke, and that’s just that. Science is about addressing WHY – why would such a pattern typify short-term desires of most heterosexual women? From the adaptation implementation perspective, the answer is steeped in our past. Women with such desires in short-term mates were more likely to leave viable offspring in the future. Mating with such “cads” likely led ancestral women who utilized short-term mating strategies to bear healthy, fit, and attractive offspring who were effective at fending off parasites (Gangestad & Buss, 1993).

So, in short, my friend who made this comment about being more attracted to Han than to Luke was completely right – it doesn’t have to be about consciously wanting to have Han’s baby over Luke’s. From an adaptation-implementation perspective, the ultimate causes of differential attractiveness toward one potential mate over another need not have any bearing on consciously trying to reproduce whatsoever. Just as fear of heights can exist without one consciously thinking about how falling a long way will lead to sudden death. Even if you don’t think that, being on the edge of a cliff in the mountains is still scary! And that’s because such fears gave our ancestors survival and reproductive benefits over others. Similarly, being sexually attracted to a potential mate may not make one think about the fitness-relevant end-product (e.g., shared offspring) – it may simply put one in a state (a hot state!) that is likely to lead to increased likelihood of mating.

And to top it off, remember, Han might be more masculine, but Luke can use the force!

References

Dawkins, R. (1976). The selfish gene. Oxford: Oxford University Press.

Gangestad, S. W., and Buss, D. M. (1993). Pathogen prevalence and human mate preferences. Ethology and Sociobiology, 14, 89-96.

Profet, Margie (1992). “Pregnancy Sickness as Adaptation: A Deterrent to Maternal Ingestion of Teratogens”. The Adapted Mind: Evolutionary Psychology and the Generation of Culture. Oxford University Press. pp. 327–365.

Schmitt, D. P., & Pilcher, J. J. (2004). Evaluating evidence of psychological adaptation: How do we know one when we see one? Psychological Science, 15, 643-649.

Shoup, M. L. & Gallup, G. G., Jr. (2008). Men’s faces convey information about their bodies and their behavior: What you see is what you get.
Evolutionary Psychology, 6, 469-479.

Anyone who has been to the Northeast is likely familiar with the miniature Dunkin Donuts convection the donut hole, aka the Munchkin. After an unsuccessful online search, I called headquarters to learn more about the history of this sweet, only to find them quite silent on the issue. What follows is based on hopeful speculation for the sake of an example of spandrel and exaptation in evolutionary theory.

Gould and Lewontin (1979) came up with the terms spandrel and exaptation to provide an explanation for the origins of heritable traits that weren’t initially adaptations. An adaptation begins as a trait that is selected for a particular function that it serves the carrier. A spandrel is a leftover of an adaptation. It has no function and is not subject to natural selection. However, if that spandrel is co-opted for a particular function, it is considered an exaptation – and then can actually become subject to selection. Though it didn’t begin as a functional product, in the end it comes to be. For example, bird feathers were initially an adaptation for thermoregulation, and later were co-opted, or exapted, for the function of flight. Flight in this case didn’t originate as an adaptation, but was co-opted from the spandrel.

The Munchkin illustrates the concept of exaptation well, though it requires a baker as “selector”, whereas natural selection operates with no selector. A doughnut in this example is a circular piece of dough with an empty circular middle. Imagine that the shape is created by making a round of dough, and then cutting out the middle piece, leaving you with the doughnut and some extra dough. Imagine further that the baker typically throws the middle piece aside as it serves no purpose. The middle piece here is a spandrel – it serves no function to the baker, but is rather a leftover portion of the functional dough – the doughnut.

However, the baker decides that those leftover pieces are too much of a waste. She decides to roll them into a ball and sell them separately from the doughnuts. She gives them a name, Munchkin, and markets them to dieters, children, and dog-owners for treats, and finds that these formerly useless pieces are now bringing in money. They have been co-opted for the function of money making, and therefore the Munchkin is an exaptation. Now she finds them so popular, the baker is creating different flavors, and fun boxes in which to sell the doughnut holes.

What originated as a mere by-product of the doughnut has now come to serve the function of a profitable treat. Though the Munchkin, as an exaptation, will be subject to selection pressures. Perhaps customers will prefer chocolate rather than plain Munchkins, resulting in more chocolate Munchkins being made. Or perhaps the mere size of the Munchkin will allow it to find its way to more diverse environments than the doughnuts, resulting in more Munchkins being made than doughnuts. Whatever the end result, the Munchkin shows that while some features are not initially subject to selection pressures, if they come to serve a function, someday they just may be.

[Postscript: I hope Stephen J. Gould had a sense of humor, otherwise he is figuratively rolling in his grave at my Just-So Munchkin story.]

Further Reading:

Buss, D. M., Haselton, M. G., Shackelford, T. K., Bleske, A. L., & Wakefield, J. C. (1998). Adaptations, exaptations, and spandrels. American Psychologist, 53(5), 533-548.

Gould, S. J., & Lewontin, R. C. (1979). The spandrels of San Marco and the Panglossian paradigm: A critique of the adaptationist programme. Proceedings of the Royal Society of London, 205(1161), 591-598.

What did Genghis Khan (circa 1162-1227) have that you don’t? He had hundreds of children and the power to absorb a vast number of tribes into his Mongolian Empire. His power can be used as an example to show that natural selection operates at the level of the individual and most often has no role in what is good for the species.

As a quick review, adaptation is the process of becoming better fit to an environment. A specific adaptation is a trait that provided its carrier with a survival and/or reproductive advantage in the past. Traits are heritable, meaning they are passed from parent to offspring. A beneficial trait is passed on more often than other traits that may prove less beneficial, and will start to characterize a subset of a species or a species – but only by way of the individual.

Let us assume that Khan’s power was a composite of heritable traits (e.g. ruthlessness, cunning, persistence), biologically passed down from parent to offspring. Power is an adaptation because it gave the possessor an increased access to resources and mates. From his wife and concubines alone, Khan is believed to have fathered hundreds of children. Indeed, a recent study found that roughly 8% of the former Mongolian Empire shares genetic material on the Y-chromosome at levels indicating the shared material isn’t due to random mutation or genetic drift, but a shared ancestor. This translates to 0.5% of the world! The shared material has been traced back about 1,000 years, around the time of Genghis Khan’s rule, and due to other circumstances is believed to be from his lineage. Thus Khan’s power helped him acquire many mates, passing on the power trait quite often. In other words, the trait benefited Genghis Khan directly – it resulted in more partial copies of himself. It was social inheritance that split Khan’s empire amongst his sons after his death; it was biological inheritance (of the power trait) that gave them the ability to expand his empire even further.

Khan’s power enabled him to invade and conquer areas stretching from the Caspian Sea to the Sea of Japan. He persuaded tens of thousands of men to join his ranks and commanded them in fierce battles. He was responsible for thousands of deaths in his quest for power and dominion over his quickly growing Mongolian Empire. His power was surely related to his vast death toll (more numerous even than his offspring) – and no one can command in such great numbers without power. In other words, the trait did not benefit the species, and in fact led to a decrease in the population of his species.

The same trait (power) that was so detrimental to the pawns in the rapidly growing Mongolian empire (e.g. part of the species) was so beneficial to Genghis Khan that he ended up with more offspring than most of us could ever imagine – and half of us (i.e. women) could ever produce in a lifetime. Thus power is a quite adaptive trait, but more importantly, explicates that natural selection operates upon what is beneficial for the individual, not the species. If Khan’s power had operated so as to benefit the pawns, and not Khan, he would not have been an effective leader in those times, and therefore he would not have left any offspring to carry on his traits.

Further Reading:

Dawkins, R. (1990). The selfish gene (2^nd ed.). Oxford: Oxford University Press.

Zerjal, T., Xue, Y., Bertorelle, G., et al. (2003). The genetic legacy of the Mongols. American Journal of Human Genetics, 72, 717-721.