What if Rev Jenyns had agreed? Part III. 'Group' selection in individuals, too.

We have been using Darwin's and Wallace's somewhat different views of evolution to address some questions of evolutionary genetics and their consequences for todays attempt to understand the biological, especially genomic, basis of traits of interest. Darwin had a more particularistic individual focus and Wallace a more group-focused, ecological one, on the dynamics of evolutionary change.

HMS Beagle in the Straits of Magellan

As a foil, we noted that a friend of Darwin's, Leonard Jenyns was offered the naturalist's job on the Beagle first, but turned it down, opening the way for Darwin. We mused about how we might think today had Wallace's view of evolution, announced in the same year that Darwin's was, been the first view of the new theory. Where we'd be now if we'd had a more group than individual focus is of course not knowable, but we feel Wallace's viewpoint, at least in some senses, has been wrongly neglected.

Population genetic theory traces what happens to genetic variants in a population over time. Almost without exception the theory treats each individual as representing a single genotype. We take individual blood samples or cheek swabs, and let our "Next-Gen" sequencer grind out the nucleotide sequences as though on a proverbial assembly line. In this sense, each individual--or, rather, the individual's genotype--is taken to be the unit of evolution.

Populations were, and generally still are, seen as a mix of these individual internally non- varying homogeneous units each having a genotype. But that's an obviously inaccurate way to view life, another reflection of the difference in viewpoint about variation in life that we've been characterizing by relating them symbolically to Darwin's and Wallace's stress in their views of evolution.

There is a strong tendency to equate genotypes with the traits they cause. This derives from the tendency to reduce natural selection to screening of single genes, because if single genes cannot be detected effectively by selection, they generally won't have high predictive value for biomedicine either. It is easy to see the issue.

But individuals are populations too
Let's ask something very simple: What is your 'genotype'? You began life as a single fertilized egg with two instances of human genomes, one inherited from each parent (here, we’ll ignore the slight complication of mitochondrial DNA). Two sets of chromosomes. But that was you then, not as you are now. Now, you’re a mix of countless billions of cells. They’re countless in several ways. First, cells in most of your tissues divide and produce two daughter cells, in processes that continue from fertilization to death. Second, cells die. Third, mutations occur so that each cell division introduces numerous new DNA changes in the daughter cells. These somatic (body cell) mutations don’t pass to the next generation (unless they occur in the germline) but they do affect the cells in which they are found.

But how do we determine your genotype? This is usually done from thousands or millions of cells—say, by sequencing DNA extracted from a blood sample or cheek swab. So what is usually sequenced is an aggregate of millions of instances of each genome segment, among which there is variation. The resulting analysis picks up, essentially, the most common nucleotides at each position. This is what is then called your genotype and the assumption is that it represents your nature, that is, all your cells that in aggregate make you what you are.

In fact, however, you are not just a member of a population of different competing individuals each with their inherited genotypes. In every meaningful sense of the word each person, too, is a i of genomes. A person's cells live and/or compete with each other in a Darwinian sense, and his/her body and organs and physiology are the net result of this internal variation, in the same sense that there is an average stature or blood pressure among individuals in a population.

If we were to clone a population of individuals, each from a single identical starting cell, and house them in entirely identical environments, there would still be variation among them (we see this, imperfectly, in colonies of inbred laboratory strains such as of mice). They are mostly the same, but not entirely. That’s because they are aggregates of cells, with genomes varying around their starting genome.

Yesterday we tried to describe why the traits in individuals in populations have a central tendency: most people have pretty similar stature or glucose levels or blood pressure. The reason is a group-evolutionary phenomenon. In a population, many different genomic elements contribute to the trait, and because the population is here and hence has evolved successfully in its competitive environment, the mix of elements and their individual frequencies is such that random draws of these elements mainly generate rather similar results.

It is this distribution of random draws of all the genetic variants in the population that determines the context and hence the success of a given variant. But the process is a relativistic one, rather than absolute effects of individual variants. Gene A's success depends on B's presence and vice versa, across the genome. There is always a small number of outliers, having drawn unusual combinations, and evolution screens these in a way that results in a central tendency that may shift over time, etc.

The same explanation accounts for the traits in individuals. There would be a central tendency in our hypothetical cloned mice. That’s because the somatic mutations generate many different cells, but most are not too different from each other. As in evolution in populations, if they are dysfunctional the cell dies (or, in some instances, they doom the whole cell-population to death, as when somatic mutations cause cancer in the individual). Otherwise, they usually comprise a population near the norm.

Is somatic variation important?

An individual is a group, or population of differing cells. In terms of the contribution of genetic variation among those cells, our knowledge is incomplete to say the least. From a given variant's point of view (and here we ignore the very challenging aspect of environmental effects), there may be some average risk--that is, phenotype among all sampled individuals with that variant in their sequenced genome. But somatically acquired variation will affect that variant's effects, and generally we don't yet know how to take that into account, so it represents a source of statistical noise, or variance, around our predictions. If the variant's risk is 5% does that mean that 5% of carriers are at 100% risk and the rest zero? Or all are at 5% risk? How can we tell? Currently we have little way to tell and I think manifestly even less interest in this problem.

Cancer is a good, long-studied example of the potentially devastating nature of somatic variation, because there is what I've called 'phenotype amplification': a cell that has inherited (from the person's parents or the cell's somatic ancestors) a carcinogenic genotype will not in itself be harmful, but it will divide unconstrained so that it becomes noticeable at the level of the organism. Most somatic mutations don't lead to uncontrolled cell proliferation, but they can be important in more subtle ways that are very hard to assess at present. But we do know something about them.

Evolution is a process of accumulation of variation over time. Sequences acquire new variants by mutations in a way that generates a hierarchical relationship, a tree of sequence variation that reflects the time order of when each variant first arrived. Older variants that are still around are typically more common than newer ones. This is how the individual genomes inherited by members of a population and is part of the reason that a group perspective can be an important but neglected aspect of our desire to relate genotypes to traits, as discussed yesterday. Older variants are more common and easier to find, but are unlikely to be too harmful, or they would not still be here. Rarer variants are very numerous in our huge, recently expanded human population. They can have strong effects but their rarity makes them hard to analyze by our current statistical methods.

However, the same sort of hierarchy occurs during life as somatic mutations arise in different cells at different times in individual people. Mutations arising early in embryonic development are going to be represented in more descendant cells, perhaps even all the cells in some descendant organ system, than recent variants. But because recent variants arise when there are many cells in each organ, the organ may contain a large number of very rare, but collectively important, variants.

The mix of variants, their relative frequencies, and their distribution of resulting effects are thus a population rather than individual phenomenon, both in populations and individuals. Reductionist approaches done well are not ‘wrong’, and tell us what can be told by treating individuals as single genotypes, and enumerating them to find associations. But the reductionist approach is only one way to consider the causal nature of life.

Our society likes to enumerate things and characterize their individual effects. Group selection is controversial in the sense of explaining altruism, and some versions of group selection as an evolutionary theory have well-demonstrated failings. But properly considered, groups are real entities that are important in evolution, and that helps account for the complexity we encounter when we force hyper-reductionistic, individual thinking to the exclusion of group perspectives. The same is true of the group nature of individuals' genotypes.

We have taken Darwin and Wallace as representatives of these differing perspectives. Had Jenyns taken the boat ride he was offered, we'd have been more strongly influenced by Wallace's population perspective because we wouldn't have had Darwin's. Instead, Darwin's view won, largely because of his social position and being in the London hub of science, as has been well-documented. A consequence is that the ridicule to which group-based evolutionary arguments have been subjected is a reflection of the resulting constricted theoretical ideology of many scientists—but not of the facts that science is trying to explain.

What needs to be worked on is not, or certainly not just, increased sample size to somehow make enumerative individual prediction accurate. For reasons we've tried to suggest, retrospective fitting to the particular agglomerate of genotypes does not yield accurate individual prediction--and here we've not even considering non-genomic aspects of each genome-site's environment. Instead, we should try to develop a better population-based understanding of the mix of variants and their frequencies, and a better sense of what a given allele's 'effect' is when we know each allele's effect is not singular nor absolute, but is strictly relative to its context both in terms of its individual and population occurrences. It's not obvious (to us, at least) how to do that, or how such an understanding might relate to whether accurate individualized prediction is likely to be possible in general.

What if Rev Jenyns had agreed? Part II. Would evolutionary theory be different from a population perspective?

In yesterday's post I noted some general differences between Darwin's individual-centered theory of evolution, and AR Wallace's more population-focused ideas.  Of course they both developed their ideas with the kinds of knowledge and technology then available, so we can use them to represent differing points of view we might hold today, but must realize that that is symbolic rather than literal. They were who they were, both skilled and perceptive, but their ideas were subject to modification with subsequent knowledge. One major piece of knowledge that emerged after their time was that genes are point causes of biological function, that is, single locations in DNA with distinct activity.
But that knowledge was derived from Mendel, Morgan, Watson, Crick and a host of others, who, following Mendel, pursued genetic function with independent point causation as the assumed starting point that drove their study designs.  DNA may be atoms on a string, but the assumption was misleading then, and still is today.

Alfred Russel Wallace

The modern theory of evolution, population genetics, is based on genes as point causes, and it recognizes the local nature of evolution in time and space.  A genetic variant's chances of spreading in a population are, naturally enough, seen in population perspective.  But by and large that perspective is about a genetic variant, and indeed attempts to explain functional and adaptive evolution from a single gene's point of view.  The variant's success depends on the relative success of other variants at the same locus--competition.  Of course that success depends on many things, but this perspective basically just 'integrates' away all factors other than the gene itself, computing a net-result picture.  It is very 'Darwinian' in the sense of being strongly deterministic and considering genes as points individually competing with each other for success.

This is not a fallacious picture, but I think it's not terribly relevant to the kinds of questions most people are asking these days, both in evolution and in biomedical genetics.  One needn't deny that individual genetic variants don't have their differential success over time, or that we can't or shouldn't be aware of nucleotide differences.  To do so would be something like denying that a house is made of bricks, the bricks can be identified and enumerated, and they have something to do with the nature of the house.  The question is the degree to which you can explain or predict the house from the enumeration of the bricks.

There are those who suggest that evolution is more about interaction at the genome level than it is about single alleles; enumerating bricks is not enough. However, the allele-focused view would have it that it is only the 'additive' aspect of each individual allele's effect on its own, that is transmitted. The idea is that even if the combination of alleles at and among loci affect an individual's traits (roughly, this is called 'epistasis'), s/he only transmits a roughly random half of those to each offspring.  Thus, the combination effect is not inherited.  Epistatic holism is an evolutionary hoax.

This venerable riposte to those arguing for a more 'holistic' or complex genomic viewpoint may be mathematically true in the abstract, but misses an important point.  In fact, the fitness (reproductive success) of a given allele entirely depends on the rest of the genome and the external environment.  If you just think about how life works (that is, metabolism, morphology, and many other complex interactions), the dependency is very unlikely to be simply additive. Things work, things adapt in combinations.  But we'll see below how this squares with the additive-only view.

In fact, the collective context-dependency of each allele's functional effects means that the evolution of a population is dependent on its mix of genomic variation--which brings us back to Wallace, and is what group selection is properly about.

Group selection: why a bad reputation?
Group selection got a bad reputation in part when a book by VC Wynne-Edwards was published in 1964 that claimed that in many species, individuals restrained their reproduction essentially for the good of the group (whether or not this was done knowingly for that purpose).  This was a kind of fitness-related altruism that was ridiculed on the grounds that if I restrain my reproduction for the good of the group, others may not be so restrained and any genetic variant that led me to do what I did would thus be out-competed.  So group selection was out, but WD Hamilton introduced concepts of extended kinship to explain altruistic behavior, such as why I might help someone at a cost to myself--if that someone were a relative, for example.  Hamilton's rule became dogma and explains much of the sociobiology of our era still today (though the rule doesn't really work very well when closely tested).

In this sense, group selection was viewed or modeled as driven by single genes and the argument was how an individual 'altruism' gene could possibly sacrifice itself and still get ahead, the one coin of the realm recognized by the most strident of Darwinists.  In recent years, various defenses of the idea and proposed mechanisms have been offered, usually with no reference to Wallace's more ecological concept.  The reason his views might be relevant is not that he thought about this in modern terms, but because he recognized that the collective qualities of the group--its overall members' traits--are what affects the group's chances of confronting the environment or other populations that it faces.

But in fact I think that while the evolution of altruism is an interesting question, it is a red herring that has given group selection a bad name.  Because there is a lot more about group selection than that gene-centered, restricted argument would suggest, and it's fundamental to life.  Indeed, it is possible that Wallace's idea, that the properties of the group determine its success, is more cogent than the gene-focused version--but for different, wholly non-mystical reasons.

Group selection, more properly conceived
The answer in brief is not a new fact but a different way of weighing the facts.  It is based on the indisputable fact that DNA is, by itself, quite an inert molecule. Anything it does is only in context.  The chance of an allele being successful depends on what else it finds itself combined with.  If in that context, the allele's effects are harmful, it has reduced prospects.  But if it finds itself in genomic and environmental circumstances in which it functions well, it can proliferate.

But what determines those genomes?  It's the relative frequency of their alleles in the population.  This is the result of the genomic history of the population as a reproducing unit.  Unless quickly removed, our new allele will see itself, probabilistically, in the company of other variants in the individuals who carry it.  If the number of those variants, and/or their frequencies, in which it can have positive effect is high enough, it has an increased chance of proliferating.  This is, in a legitimate sense group selection, because genomewide the success of the group depends on its collective distribution of alleles.  (Here we're not considering how that collective success operates, whether in terms of mating, avoiding predators, finding food, dealing with local climate, etc.).

The same variant that does very well in one genomic or environmental setting may do very poorly in another.  This is another manifestation of the central fact that a variant has no predetermined effect on its own.  It's why personalized medicine, based on predicting disease from genotypes, has a long way to go, at best, for other than very severe, largely early onset traits.

It is not that the individual variant, or the individual person, isn't important, or that we can't trace the frequency change of the variant, just as has been done for decades by population genetics theory.   But it misses the important collective aspect of an allele's success.  It's like the fact that we can count the bricks that make up our building, but we are hard-pressed to understand the building that way.

Over time, a successful population accumulates enough variants in enough genes that enough newly arising alleles are in favorable 'soil' to confer viable effects on individuals who bear them.  A population depauperate of enough of an allelic mix, genomewide, dies out.  This is, in every meaningful and non-mystical sense, a group phenomenon and if the term hadn't already been abused, group selection.  If a population perspective is really the most important one for understanding genome dynamics, then our usual genetic reductionism is misplaced.  

The Normal (bell-shaped) distribution of so many traits, like stature; UConn WWI recruits

Everyone in a population differs a bit but most people, for most traits, are rather near the middle.  The roughly Normal (bell-shaped) distribution of traits like human stature is a reflection of this.  There are those in the high- or low-end tails (very tall or very short), but most are near the middle.  There is a strong 'central tendency'.  Where does that come from?  It is a direct reflection of an evolution that makes most people inherit what in their collective ancestry has evolved as a 'fit' state for that population's circumstances.  There are always new mutational variants arising, and if the population--the 'group'--had not evolved this central tendency, it would not be a healthy one, and that would affect the likely fate of new mutations.  There are exceptions, but the restricted variance of natural populations, the tendency of most individuals to be quite similar, reflects what is, in fact, a form of group-selection history.

A major way in which this can arise, given that we have genomes made of multiple chromosomes and there is recombination and we are diploid but pass on only half our genome complement, is for many different genomic factors to affect a trait--for it to be 'polygenic'.   I think that it is the assembly of many more or less equivalent parts, independently segregating, that enables most individuals to inherit what the population's previous history has proved viable, that is, multiple independent contributors is why such central-tendency, limited-variance characteristics are so widespread.  Gene duplication and other processes help generate this state of affairs.  It's the way molecular interaction works; if things had been too genetically unitary, survival would have been more precarious.

From this perspective, the standard 'selfish gene' viewpoint's denial of the importance of epistasis and other contextual elements of gene function is off the mark.  It misperceives the nature and vital importance of the population in which these combinations exist, and the necessity that those factors be there, in enough numbers and/or with high enough frequency.

So, Wallace again?  But wait--isn't it individuals who reproduce or not?
But what about those individuals, on whom a century of population geneticists and countless popular science writers, have placed their hyper-competitive hyper-individualized stress?  The individual, driven by some critical genetic variant survives or not.  Individuals as wholes are viewed (or should we say dismissed), essentially, as mere carriers of the gene whose evolution is being tracked.  The context of population may be real, as discussed above, but the individual, basically a manifestation if its genotype, is what selfishly acts and determines success. No?

Sure, in a sense.  But the variant's prospects depend on the collective, and it's mutual, or relative.  Variant One is affected by Variant Two--but Variant Two is affected by Variant One, and so on.  The individual, or worse, individual gene focus is something one can compute, but it is misleading.  And, in fact, the situation is even more problematic in respect to what individuals actually are, genomically.

In Part III, I'll discuss how individuals, too, are being misperceived as the ultimate functional units based on their individual genotypes, either as wholes or in terms of specific genes.  Again a group or population perspective has an important, largely unrecognized role to play in individuals' and hence groups' success.

Wallace was onto something that's rather absent in Darwin, and still absent today as a result of the fact that the particularist aspect of Darwin's and Mendel's view prevailed.

What if Rev Jenyns had agreed? Part I. Would evolutionary theory be different?

In 2006 I wrote an article about the long potential impact that historical quirks can have on science, based on the fact that in 1831 an Anglican cleric named Leonard Jenyns said "no, thanks" to an offer. It so happened that that offer was to be the naturalist on a surveying voyage to be undertaken by the Royal Navy. But Jenyns was interested in natural history as a hobby, rather than as a career, and he said he had to spend time with his parishioners and couldn't be away for the long years of such a voyage. He might also have used that as an excuse to avoid the known dangers of such trips at the time.

Leonard Jenyns, the reluctant reverend

Leonard Jenyns, the reluctant reverend

Too bad, said John Henslow at nearby Cambridge University, who had recommended Jenyns. So he recommended another of his students, a fellow named Charles Darwin. Darwin was interested in natural history, too, but spent most of his time riding and shooting, as did most members of his social class, and it wasn't clear that he'd make a serious enough candidate for the position. But, after agonizing and consulting family, Charles said "Yes!" The ship was, of course, the Beagle, and the voyage was to shake the world.

I've written about this incident before (Evol. Anth., 15:47-51, 2006) because it is interesting to surmise about how biology, in particular evolutionary and genetic theory and approaches, might be today if Jenyns had agreed, and Darwin had gone fox-hunting during those important years. What might have been different? Wouldn't we have eventually ended up where we are today, celebrating Jenyns rather than Darwin? I think definitely not.

Jenyns was basically a biblical fundamentalist, which meant a creationist.  He would have gotten along famously with Captain FitzRoy, also a strong believer.  Debates (after grace) over wine and meals would not have been about the origin and distribution of variation in plants and animals.  But can we doubt that we’d have learned about evolution anyway?  No, not at all.

At roughly the same time period, another not-so-wealthy naturalist was doing his natural history in remote parts of the world (first Amazonia, then Indonesia), and he developed a clear idea of the ‘transmutation’ of species on his own.  In 1858 he sent a brief manuscript explaining his idea to a correspondent, one who had become well-known among British naturalists, the same Charles Darwin. 

This stunned Darwin who had been working ploddingly on his own theory of evolution.  But with very good grace, he hastily assembled some bits and pieces to show his ideas (and, perhaps not so incidentally, his priority) which along with Wallace’s manuscript were read to the Linnaean Society.  The world had been told, but hardly anyone was listening until the following year when Darwin published his lengthy assertion of the idea that the diversity of life arose through a gradual historical process—his Origin of Species.

Both Darwin and Wallace were famously influenced by economist Thomas Malthus’ book arguing the inevitable pressure of growing population on available resources, and that idea led to the idea that it was competition for such resources in Nature that inevitably favored (selected) those better competitors in terms of their future reproductive success.  Adaptation by natural selection was the process that they argued explained the diversity and functional traits of species.

But the two ideas were rather different

Darwin and Wallace placed very different stress on how this process worked.  Darwin stressed competition among individuals for survival or mates, so that in a given location the better-endowed individuals would have all the fun at the expense of their less-suited contemporaries.  Since traits of organisms were at that time viewed as caused by the deterministic effects of some causal elements (that, in his way, the Moravian monk Gregor Mendel was studying, unbeknownst to Darwin and Wallace).  The most successful competitors would transmit these elements to their offspring, and the elements would thus proliferate over time to replace less-successful elements.

Differential success was also important to Wallace.  He recognized that, of course, individuals proliferate well or not, but his stress was more on competiton among groups or species, and/or of groups against the limits of their environment.  Some groups would do well and modify as successfully adapted species while others would wane.  It was the group characteristic, even though of course comprised of individual members, that told the tale.

Now, if Darwin had stuck to his guns, so to speak, we would be talking today of Wallacian, not Darwinian, evolution.  Whatever we would have discovered about the nature of inheritance, whether or not by now we had discovered DNA and its functions in the cell, we may very well not have developed our ferocious obsession with individual competition, an obsession that often drives us to view genes as if they themselves, rather than the whole individuals or whole populations or whole species, were the central competitors in the evolutionary race.

I think things today might be very different, and we might not be trying to enumerate individual genes in individuals’ genotypes when it came to accounting for genetic causation, genomic and even adaptive evolution.  The reason isn’t that individuals and their genotypes are unimportant, nor that some mysterious function unrelated to individual genes reifies the concept of population to give one population an edge over another.  The reason would simply be a different way to understand that the dynamics of both individuals and their genes are fundamentally aggregate phenomena.  And we’d have very different ideas on the role of populations and context.

In Part II, I’ll consider the collective nature of genomes in populations and how that affects their evolution in group-contextual ways.  Then in Part III, I'll try to show that individuals are themselves similarly context-driven populations of genotypes.

Is it competition vs cooperation; or, cooperation lets competition be?

Since Darwin, emphasis in evolutionary theory has been on competition between individuals and species in the race for optimal fitness -- he or she who passes the most genes to subsequent generations wins.  Darwin saw this through the lens of the rampant cruelty of Nature, and the need for individuals to find food and mates and escape being eaten.

To many, this is a fundamental underpinning of evolution, although in recent years a number of evolutionary biologists have begun to think that perhaps cooperation deserves a larger role.  We have done our part, in our book (titled, in fact, The Mermaid's Tale: Four Billion Years of Cooperation in the Making of Living Things) and here on MT and elsewhere, though, despite our best efforts, competition remains the predominant view of how life works.

In our book we suggest that cooperation is a fundamental principle of life, arguably much more pervasive and important than competition because it happens at all levels all the time, from minuscule intracellular spaces to grander ecosystems, instantaneously as well as over evolutionary time.  It is, we think, hard to argue that competition plays such a central role.

A friend and sometime co-blogger Reed Goodman alerted us to an interesting piece the other day in The Baffler, "What's the Point if You Can't Have Fun?" by David Graeber.  Graeber, currently Professor of Anthropology at the London School of Economics, believes that behavioral scientists have gone over the top in arguing that there must be a rational purpose to every animal behavior.  

I’m simply saying that ethologists have boxed themselves into a world where to be scientific means to offer an explanation of behavior in rational terms—which in turn means describing an animal as if it were a calculating economic actor trying to maximize some sort of self-interest—whatever their theory of animal psychology, or motivation, might be.

Instead, why can't they just be having fun?  

Graeber notes that with the discovery of genes, evolutionary theorists quickly adopted the idea that everything animals did was in the service of passing along their own genes, an idea popularized by Richard Dawkins' in his book The Selfish Gene, but also widely accepted within evolutionary biology as well.  Indeed, evolutionary biologists tend to smell a competitive rat everywhere, nurturing the view that everything animals do must be adaptive, naturally selected, and for the purpose of out-reproducing the competition. 

This of course raises problems like altruism, cooperation among non-kin, animals sacrificing their own life for someone else, and so forth, but these have generally been hand-waved away with we would say rather contorted arguments that reframe kindness, cooperation and self-sacrifice as just competition in disguise.  Of course, that implicitly makes a tautology of every such explanation, based on an axiom -- an assumption -- of pervasive selective determinism.

Graeber isn't at all a fan of this strict view of biology and evolution.  His essay is wide ranging in scope,  from inchworms dangling in air for the sheer fun of it, to the historical context in which the idea that the purpose of life is the propagation of DNA (our genes thus made us invent the PCR machine, for  unlimited propagation of DNA?) could gain purchase, to the discussion of free will and consciousness.  It is provocative and well worth a read.  

But it was Graeber's mention of a 1902 book by Russian naturalist Peter Kropotkin (1842-1921) that most caught my eye.  In Mutual Aid: A Factor of Evolution Kropotkin argues that Darwin was wrong to place so much emphasis on competition, because cooperation -- mutual aid -- is so obviously in evidence all around us.  The idea of the struggle for life as a 'law of nature' was something he just couldn't accept because, as he wrote "...I was persuaded that to admit a pitiless inner war for life within each species, and to see in that war a condition of progress, was to admit something which not only had not yet been proved, but also lacked confirmation from direct observation." 

As a naturalist, Kropotkin spent much time traveling and observing nature. In Mutual Aid he documents  evidence of aid over conflict among animals, in humans and throughout human evolution and history, writing:

As soon as we study animals -- not in laboratories and museums only, but in the forest and prairie, in the steppe and the mountains -- we at once perceive that though there is an immense amount of warfare and extermination going on amidst various species, and especially amidst various classes of animals, there is, at the same time, as much, or perhaps even more, of mutual support, mutual aid, and mutual defense amidst animals belonging to the same species, or at least to the same society.  Sociability is as much a law of nature as mutual struggle.  

But which comes first, evidence or interpretation?

Kropotkin was a prominent figure in 19th century activist politics.  He was, according to the wisdom of the masses, a "geographer, economist, activist, philologist, zoologist, evolutionary theorist, philosopher, writer and prominent anarchist." (Wikipedia.)  He was sympathetic to the plight of the peasant in Russia as a young man, and to socialist ideas, though he eventually settled on anarchism and as a political activist, was imprisoned for subversive activities in 1876.  He escaped from prison before his trial, however, and fled to Europe, only returning to Russia after the revolution in 1917, enthusiastic about the changes he saw happening, though eventually disillusioned by the authoritarian socialism that the revolution became.

Kropotkin disliked capitalism and the idea that life must be a struggle.  As an anarchist, he preferred to believe that humans were capable of mutual aid and cooperation, and that we could effectively run our own societies.  On the other hand, competition was in the cultural air when Darwin was doing his thinking, with the British empire dominating much of the world, the beginning of the industrial age and the rise of capitalism, the economics of Thomas Malthus who was so influential to Darwin's thinking, so it was perhaps natural that Darwin, and Wallace too -- and indeed Richard Dawkins in the 1970's -- framed their theories of evolution in terms of competition.

One can assert that if Kropotkin was driven by his ideology to see in Nature what his filters allowed him to see, then the same certainly applies to the Darwinians and even to the gentle Charles himself.  If Darwin's view prevailed in the west, the cooperation-based views of Lysenko prevailed in the Soviet Union, with disastrous consequences for science.  But viewed in its context, these polarities are understandable. 

What does this say about which view is right?
I don't know.  Ken and I thought we were writing  The Mermaid's Tale about biology.  As we wrote in the book, competition and cooperation are laden words, but we explicitly chose 'cooperation' as an antidote to 'competition' with all its political and cultural meaning.  More neutral and scientifically appropriate terms like 'successful interaction' and 'differential proliferation' would serve science better and be less a matter of defining everything before it's observed.  However, our intention was to describe cooperation not just as kindness, but cooperative interactions among genes, organelles, organs, organisms and species.  In that context, we had little to say about culture, except insofar as we would argue that culture generally and manifestly usually trumps genetically driven behaviors.

So, I was surprised (and of course pleased) to see a recent review of our book on Amazon that says, among other things, "Would more anthropologists and policy makers read this…".  It's a favorable review, so presumably the author sees political and cultural meaning where we were explicitly only intending to describe biology.

But that's okay, and as it should be.  Science is always done in cultural or political context.  To a great extent, we see what we believe.  

Selecting people

On natural selection in humans
In the Rival del Garda meeting we were happy to see Luca Cavalli-Sforza for the first time in many years. Luca, a towering figure in human genetics in the last third of the 20th century, was one of the most important conceptual leaders in uniting population (evolutionary) genetics, along with culture and language, in accounting for current human diversity. Luca, long at Stanford but who retired back home in Italy a few years ago, is well into his '80s, but still spry enough and intellectually lively. Ken had interacted with him extensively in the past, including a mid-70s sabbatical in his lab at Stanford, and subsequently in the attempt to organize a global human genome diversity project (HGDP).

Luca gave a talk at the meeting on natural selection in humans. We wondered whether, at his age and removal from Stanford he could really be up to date with the huge, rapidly emerging literature on searches of the human genome for signatures of selection. Intense, highly technical genomewide comparison of variation between humans and other primates, but especially among human continental groups, has been undertaken by many investigators using HGDP-like samples and the genetic variation in the HapMap project.

There, the idea is to find genes or genome regions in which variation is reduced in ways suggesting that specific selection has taken place--such as to produce lighter or darker skin color in various continents and/or climates, or the ability of humans to resist malaria, or of adults to digest milk (these are the classic examples).

Such searches are for classically Darwinian effects. That is, they're about who in a population has higher 'fitness'--net reproductive success because they survive better or simply have higher fertility. The search is difficult and only a few specific instances have been found, for reasons too much to go into in this post. But there is at least widespread belief that there's been quite a lot of such selection since we spread out from our African ancestral home to become a globally distributed species: how could we inhabit the globe's diversity of environments without this being the result of natural selection?

Well, Luca surprised us. His point was about culture rather than genes per se. He quite correctly noted that our having culture helped us adapt quickly to diverse environments (clothing and fire, rather than fur, to protect against cold, for example, or language to communicate among coordinated hunters or gatherers).

Non-Darwinian group selection
Luca's evidence was thus entirely unrelated to the current genomewide statistical searches, but instead related to our rapid global expansion that could not be explained by genes--except by our species' shared genes related to thinking ability, that made us capable of culture.

Humans have clearly expanded rapidly at the expense of other species. We have invaded every environment, and displaced other species where needed, advancing some such as cattle or wheat for our own use instead. Our numbers have increased in a few thousand years from a few thousand to a few billion. Nothing could be clearer as proof of natural selection in humans.

However, this is not Darwinian selection in the usual sense! Instead it is a kind of group selection, the favoring of our group vis-a-vis groups of other species that we displaced. It is closer to the version of selection and evolution proffered by Alfred Wallace (who came to his ideas independently of Darwin). Wallace gave more stress to group competition and group struggle against environments, while Darwin clearly and strongly stressed competition among individuals within groups.

The two are not incompatible at all, and both processes can be occurring at any or every time. But it's not what people have in mind these days, in their frenetic hunt for good and bad genes. So Luca may or may not be up to date in that area of work, but he certainly pointed out what is, for our species, clearly and by far the most important aspect of selection involving humans! Far more important than the rather minor kinds of selection we know about at the specific gene level--even including malaria and skin color effects.

Politically correct, if scientifically incorrect
However, in stressing this view, Luca went on to argue that because selection in humans was culture-based, there was little evidence for racial differences that could be attributed to selection. Race differences (here, let's ignore the problems with the term 'race'), he said, are superficial only. They don't reflect natural selection beyond such traits as skin color. The argument is one Luca has been making for decades, as he has been perhaps by far the leader in trying to relate human genetics to human culture, such as correlating language with geography with genetic variation. But his argument unfortunately reflected a quite out-dated view, that in some ways can even be said to be politically correct, if scientifically incorrect. To see why, let's look at the case that was made.

Luca has long pointed out that, to a considerable degree, human genetic differences are correlated with geography. The farther apart geographically that two people are (here, we refer to 'indigenous' people rather than recent intercontinental migrants), the more different they are genetically. This is called 'isolation by distance.' There is quibbling about the details, but the idea is basically accurate: French and Swedish people are genetically more like each other than French and Koreans are. This, Luca argued, shows that there cannot be much due to natural selection, because selection is related to local environmental conditions, which can be very different in nearby regions, or very similar in distant regions, would not leave such a generic pattern of differences.

But there's a subtle fallacy here. Selection of a given trait affects only the genes that produce that trait, not the whole genome. Even if selection is affecting all genes at all times, each gene is affected by different environmental conditions. And selection works not with global variation, but only with variation present in any local area. Thus, even with selection, we see isolation by distance effects.

More importantly, isolation by distance is studied by using genomewide variation. There is often a deliberate choice of genetic variants that are thought not to be involved in functionally important traits (so-called selectively neutral parts of the genome), and hence variants that are not involved in selection. Isolation by distance in the genome overall, especially at such neutral regions, is perfectly compatible with all sorts of selection going on at individual genes, but differently in different world regions.

We can see this easily in another way. Two people can have a trait, like blue eyes, diabetes, or color blindness for the same genetic reason. As a rule, the same genetic variant found in two people are descendant copies of a single original mutation that occurred sometime in the past. In that sense, they are close relatives at that particular gene. But if you look at genomewide variants, they will have no particular relationship relative to other people in the population.

So, whatever you think about the pervasiveness or importance of natural selection in the history of different human 'races', the isolation by distance argument is basically irrelevant.

Thus, while the massive global expansion of humans is overwhelming and persuasive evidence for culture-based group selection favoring humans, the global human expansion is perfectly compatible with all sorts of local selection taking place. How much of that has actually happened is a separate question requiring its own kind of evidence; and so far, that evidence has been very hard to come by.

Origin of species?

2009 is being celebrated as the 150th anniversary of Charles Darwin's famous book On the Origin of Species . . . . whose full title continued by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life. Actually, 2008 was a more legitimate anniversary to celebrate, because it was a year earlier that Darwin's and Alfred Wallace's papers suggesting that species arose by the action of natural selection were read before the Linnaean Society in London.

We rightly celebrate Darwin's contribution to science, which clearly was among the most incisive, sweeping, and transformative scientific revolution that has ever occurred. The theory of evolution by natural selection has become the clear core of most of the life sciences, and its ideas have been borrowed by social and physical sciences--even by cosmology and astronomy (yes! where universes are seen as competing ecologies of galaxies, coming and going via black holes, based on their basic properties, etc.).

But was the Darwinian theory correct?

Natural selection is certainly a phenomenon of life, and it can lead to changes in traits whose basis is heritable (generally, this means is 'genetic', or encoded in DNA). Darwin equated that with the same process that leads to speciation. Over time, organisms become differentiated by virtue of the adaptive differences that arise by natural selection in different environments, and these adaptive differences make for new species. Clearly this can in principle lead to mating incompatibility, the criterion usually accepted as a definition of species, and once mating no longer occurs the populations, that started out as one, can diverge more and more. Hence, over very long time periods, we have sea creatures diverging into fish, reptiles, and mammals. Indeed, we have plants and animals diverged from single ancestral species.

But the relevant questions these days does not have to do with divergence from common ancestry nor how traits might evolve, nor even the definition of species, but the process of speciation itself. That is still not well answered, and facile Darwinian explanations don't work nearly as well as they are said to. In fact, in many ways they are as vague and assumption-bound -- and perhaps as wrong! -- as they were in Darwin's day, and for the same reason.

When populations are separated for long time periods, genetic differences arise among them. Mutations occur locally in each population, but they are relatively rare and basically unique at the DNA level. That's because the very same mutation, say an A to a G at some specific spot in DNA, only occurs once in every ten to hundred million parent-offspring transmissions, roughly speaking. Populations in each region occupied by a species will accumulate such differences across their entire genomes. These changes will have a range of effects -- some none at all, others affecting the organism's traits. Selection may or may not prefer one version over the other.

The upshot is that regional differences arise. Darwin thought these were mainly due to selection's screening of the variants, leading to different local adaptations in populations of what had been a single species, and hence to mating barriers.

This is true only if the changes affect mating compatibility, because sperm fails to fertilize eggs, or the individuals don't choose to mate, etc. But just having, say, different shaped beaks doesn't mean you can't or won't mate (if you're a bird). In fact, humans occupy the proverbial ends of the earth, and those in Tierra del Fuego have been isolated from those in southern Africa for fifty to a hundred thousand years (or more), they look very different, their genomes are so different that one would never mistake a Fuegian for a San. Yet they are sexually compatible. The same is true of baboon species that have been separated for millions of years. In both these primate examples, the regional genetic differences are genome-wide, not just in a gene here and there. And these are just a couple of many examples.

Yet the opposite can also be true. Ring species are those occupying a long linear region, in which individuals from adjacent parts of the range are mating-compatible, but individuals from the ends of the range are not. Yet, these are considered the same species. Ring species show the subtle nature of speciation (and, by they way, humans have not become a ring species despite long separation).

At the same time, single mutations can make mating incompatible in what are otherwise clearly the same species. Known mutations of this type are called 'hybrid sterility' mutations and several examples have been studied. Single mutations or chromosomal changes can lead to mating incompatibility, and hence effectively set up different species, with no other 'adaptive' changes in the Darwinian sense. Likewise, a substantial fraction of human matings, even within a single population (e.g., infertile marriages) shows that the usual kinds of physical and behavioral traits need not arise by Darwinian processes, in order for new species to form. Unless, of course, one wants to 'save' classical Darwinism as a dogma by defining the responsible mutations as being 'adaptively' different. Nothing we've said here invalidates the ideas of common ancestry and the potential of natural selection to mold traits, and mating-incompatibility mutations may literally be viewed as 'adaptations', but that distorts the meaning of adaptation and natural selection.

These are profound facts. They show that there are still many important problems, central problems, to work on in biology. Despite Darwin's brilliant insights, some of his basic reasoning and objectives were not as correct as they have been viewed for 150 years.