Thursday, May 3, 2018

Perhaps Humans Are One Giant Kluge (Genetically Speaking)

Disclaimer:  I am now retired, and am therefore no longer an expert on anything.  This blog post presents only my opinions, and anything in it should not be relied on.
Over the past year, among other pastimes, I have read several books on the latest developments of genetics and the theory of evolution.  The more I read, the more I feel that my background in programming offers a fresh perspective on these developments – a somewhat different way of looking at evolution. 
Specifically, the way in which we appear to have evolved to become various flavors of the species Homo sapiens sapiens suggests to me that we ascribe far too much purpose to our evolution of various genes.  Much if not most of our genetic material appears to have come from a process similar to what, in the New Hacker’s Dictionary and more generally used computer slang, is called a kluge.
Here’s a brief summary of the definition of kluge in The New Hacker’s Dictionary (Eric Raymond), still my gold standard for wonderful hacker jargon.  Kluge (pronounced kloodj) is “1.  A Rube Goldberg device in hardware/software, … 3.  Something that works for the wrong reason, … 5. A feature that is implemented in a ‘rude’ manner.”  I would add that a kluge is just good enough to handle a particular case, but may include side effects, unnecessary code, bugs in other cases, and/or huge inefficiencies. 

Our Genes as a Computer Program

(Note: most of the genetics assertions in this post are plundered from Adam Rutherford’s “A Brief History of Everyone Who Ever Lived”)
The genes within our genome can be thought of as a computer program in a very peculiar programming language.  The primitives of that language are proteins with abbreviations A, G, C, and T.  The statements of the language, effectively, are of form IF (state in the cell surrounding this gene is x AND gene has value y THEN (trigger sequence of chemical reactions z, which may not change the state within the cell but does change the state of the overall organism).  Two peculiarities:
1.       All these gene “statements” operate in parallel (the same state can trigger several genes).
2.       The program is more or less “firmware” – that is, it can be changed, but over short periods of time it isn’t. 
Obviously, given evolution, the human genome “program” has changed – quite a lot.  The mechanism for this is mutation:  changes in the “state” outside an instance of DNA that physically change A, G, C, T, delete or add genes, or change the order of the genes in one side of the chromosome or the other.  Some of these mutations usually occur within the lifetime of an individual, during the time when cells carry out their programmed imperatives to carry out tasks and subdivide into new cells.  Thus, one type of cancer (we now know) is caused when mutation deletes some genes on one side of the DNA pairing, resulting in deletion of the statement (“once the cell has finished this task, do not subdivide the cell”).  It turns out that some individuals are much less susceptible to this cancer because they have longer chains of “spare genes” on that side of the DNA, so that it takes much longer for a steady statistically-random stream of deletions to result in statement deletion.

Evolution as an Endless Series Of Kluges

Evolution, in our computer-program model, is new (i.e., not already present somewhere in the population of the species) mutations.  The accepted theory of the constraints that determine what new mutations prosper over the long run is natural selection. 
Natural selection has been approximated as “survival of the fittest” – more precisely, survival of genes and gene variants because they are the best adapted to their physical environment, including competitors, predators, mates, and climate, and therefore are most likely to survive long enough to reproduce and out-compete alternative mates.  The sequencing of the human genome (and that of other species) has given us a much better picture of evolution in action as well as human evolution in the recent past.  Applied to the definition of natural selection, it suggests somewhat different conclusions:
·         The typical successful mutation is not the best for the environment, but simply one that is “good enough”.  An ability to distinguish ultraviolet and infrared light, as the mantis shrimp does, is clearly best suited to most environments.  Most other species, including humans, wound up with an inability to see outside the “visible spectrum.”  Likewise, light entering the eye is interpreted at the back of the eye, whereas the front of the eye would be a better idea.
·         Just because a mutation is harmful in a new environment, that does not mean that it will go away entirely.  The gene variant causing sickle-cell anemia is present in 30-50% of the population in much of Africa, the Middle East, the Philippines, and Greece.   Its apparent effect is to allow those who would die early in life from malaria to survive through most of the period when reproduction can happen.  However, indications are that the mutation is not disappearing fast if at all in offspring living in areas not affected by malaria.  In other words, the relative lack of reproductive success for those afflicted by sickle-cell anemia in the new environment is not enough to eradicate it from the population.  In the new environment, the sickle-cell anemia variant is a “bug”; but it’s not enough of a bug for natural selection to operate.
·         The appendix serves no useful purpose in our present environment – it’s just unnecessary code, with appendicitis a potential “side effect”.  There is no indication that the appendix is going away. Nor, despite recent sensationalizing, is red hair, which may be a potential side effect of genes in northern climes having less need for eumelanin to protect against the damaging effects of direct sunlight.
·         Most human traits and diseases, we are finding, are not determined by one mutation in one gene, but rather are the “side effects” of many genes.  For example, to the extent that autism is heritable (and remembering that autism is a spectrum of symptoms and therefore may be multiple diseases), no one gene has been shown to explain more than a fraction of the heritable part.
In other words, evolution seems more like a series of kludges:
·         It has resulted in a highly complex set of code, in which it is very hard to determine which gene-variant “statement” is responsible for what;
·         Compared to a set of genes designed from the start to result in the same traits, it is a “rude” implementation (inefficient and with lots of side-effects), much like a program consisting mostly of patches;
·          It appears to involve a lot of bugs.  For example, one estimate is that there have been at least 160,000 new human mutations in the last 5,000 years, and about 18% of these appear to be increases in inefficiency or potentially harmful – but not, it seems, harmful enough to trigger natural selection.

Variations in Human Intelligence and the Genetic Kluge

The notion of evolution as a series of kluges resulting in one giant kluge – us – has, I believe, an interesting application to debates about the effect of genes vs. culture (nature vs. nurture) on “intelligence” as measured imperfectly by IQ tests. 
Tests on nature vs. nurture have not yet shown the percentage of each involved in intelligence variation (Rutherford says only that variations from gene variance “are significant”).  A 2013 survey of experts at a conference shows that the majority think 0-40% of intelligence variation is caused by gene variation, the rest by “culture”.  However, the question that has caused debate is how much of that gene variance is variance between individuals in the overall human population and how much is variance between groups – typically, so-called “races” – each with its own different “average intelligence.” 
I am not going to touch on the sordid history of race profiling at this point, although I am convinced it is what makes proponents of the “race” theory blind to recent evidence to the contrary.  Rather, I’m going to conservatively follow up the chain of logic that suggests group gene variance is more important than individual variance. 
We have apparently done some testing of gene variance between groups.  The second-largest variance is apparently between Africans (not African-Americans) and everyone else – but the striking feature is how very little difference (compared to overall gene variation in humans) that distinction involves.  The same process has been carried out to isolate even smaller amounts of variance, and East Asians and Europeans/Middle East show up in the top 6, but Jews, Hispanics, and Native Americans don’t show up in the top 7. 
What this means is that, unless intelligence is affected by one or only a few genes falling in those “group variance” categories, most of the genetic variance is overwhelmingly likely to be individual.  And, I would argue, there’s a very strong case that intelligence is affected by lots of genes, as a side-effect of kluges, just like autism.
First, over most of human history until the last 250 years, the great bulk of African or non-African humans have been hunters or farmers, with no reading, writing, or test-taking skills, and with natural selection for particular environments apparently focused on the physical (lactose tolerance for European cow use) rather than intelligence-related (e.g., larger brains/new brain capabilities).  That is, there is little evidence for natural selection targeted at intelligence but lots for natural selection targeted at other things. 
Second, as I’ve noted, it appears that in general human traits and diseases usually involve large numbers of genes.  Why should “intelligence” (which, at a first approximation, applies mostly to humans) be different?  Statistically, it shouldn’t.  And as of yet, no one has been even able to find one gene significantly connected to intelligence – which again suggests lots of small-effect genes.
So let’s imagine a particular case.  100 genes affect intelligence variation, in equal amounts (1% plus or minus).  Group A and Group B share all but 10 genes.  To cook the books further, Group A has 5 unique plus genes, and Group B 5 unique minus genes (statistically, they both should have equal amounts plus and minus on average).  In addition, gene variance as a whole is 50% of overall variation.  Then 10/95 of the genetic variation in intelligence (about 10.5%) is explained by whether an individual is in Group A or B. This translates to 5.2% of the overall variation being due to the genetics of the group, 44.8% being due to individual genetic variation, and 50% being due to nurture.
Still, someone might argue, those nature vs. nurture survey participants have got it wrong:  gene variation explains all or almost all of intelligence variation.  Well, that still means that nurture has 5 times the effect that belonging to a group does.  Moreover, under the kluge model, the wider the variation between Race A and Race B, between, say, Jewish-American and African-American, THE MORE LIKELY IT IS THAT NURTURE PLAYS A LARGE ROLE.  First of all, “races” do not correspond at all well to the genetic groups I described earlier, and so are more likely to have identical intelligence on average than the groups I cited.  Second, because group variation is so much smaller than individual variation, group genetics is capable of much less variation than nurture (0-10.5% of overall variation, vs. 0-100% for nurture).  And I haven’t even bothered to discuss the Flynn Effect, which is increasing intelligence over time, equally between groups, far more rapidly than natural selection can operate – a clear indication that nurture is involved.
Variation in human intelligence, I say, isn’t survival of the smartest.  It’s a randomly distributed side effect of lots of genetic kluges, plus the luck of the draw in the culture and family you grow up in.

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