Showing posts with label genetics. Show all posts
Showing posts with label genetics. Show all posts

Wednesday, April 27, 2022

Reading New Thoughts: The Possible Death of Race (Verny, “The Embodied Mind”)

 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.

Thomas Verny’s “The Embodied Mind” would appear at first glance to have nothing to do with genetics or “race”/ethnicity.  It is, in fact, an interesting attempt to argue that memory, thought, and even consciousness takes place in other areas of the body besides the mind.  However, as part of its argument that memories can be passed from generation to generation, it takes a detailed look at recent research in epigenetics – including both animal experiments and human analyses.   And from this, I have concluded that it is reasonable to draw some brief initial conclusions about the role that epigenetics plays in differential inheritance of characteristics.

So let me lay out, first, the overall model of inherited or socially influenced differences that I see as underlying recent research, more or less, and then discuss how I see this research impacting our whole notion of race and ethnicity as factors in such areas as intelligence (however defined), success in life (however defined), and physical skills.

The Disruptive Effect of Epigenetics in Theory

Crudely speaking, I used to sense that the theory of evolution reduced causes for differences into two:  genes (which are inherited and are slow to change because they involve mutations that “crowd out” existing genetic structure because they are better fitted to a new physical environment) and society (behaviors and skills learned from others, typically relatives).  Thus, absent concrete knowledge of the genome, it was possible that all differences between groups could be explained by differences in genes, and it was possible that none of it could be explained by genes.

The first major disruption to the wealth of research trying to determine how much could be explained by genetics, I think, was the sequencing of the genome.  This and follow-on research establish that 99% of the human genome is identical, and that while physical appearance (e.g., eye, hair, and skin color) and a few diseases or disorders (e.g., sickle-cell anemia)  still seemed to be clearly genetically based, almost everything else could not be explained genetically by less than 10-20 “different” genes or even no matter how many “different” genes one tried to use as a combined explanation.  Moreover, when one tried to group by so-called “race” or ethnicity, then the research tended to show that the maximum difference in genes was between African and all other groupings, with steadily decreasing differences between Asian, European, American, and Polynesian groupings – clearly explained by the fact that Africans had remained in the same physical environment over the last 50,000 years, with relatively little cross-breeding, while the others had typically moved at least once to a different physical environment in the intervening 50,000 years.  So even where differences in genes might be held to explain performance or skills, for all but the crudest grouping the differences across groups were much less than the <1% maximum.

And then, along came epigenetics. 

What was different and puzzling about epigenetics can be encapsulated in one research result:  There are two groups of one species of fish in different areas of a coral reef with absolutely identical genes – but different physical characteristics (a skin tag in one group, no skin tag in the other). 

The explanation for this, it turns out, is that epigenetics acts like an on-off switch or cap-off/cap-on for a gene or genes.  Flip the cap off, and the gene “expresses” itself in physical characteristics in a new way; flip the cap back on, and the gene goes back to the old “expression”.  These “switches” reside in so-called “junk” DNA, in RNA, and in proteins associated with the workings of the genes.  And, as the research result cited above indicates, they are inheritable, down to (as far as studies have gone) the fourth generation.  What remains unclear is just how a switch that is turned on gets turned off again; it is still possible that it only does so via cross-breeding with those whose gene is not so expressed and/or “crowding out” the inheritors as a smaller and smaller part of the population. 

So epigenetics appears to disrupt “nature vs. nurture” discussions, I think, in two ways:

1.       It appears at first glance to indicate that, even if some difference in characteristics is not explainable by the action of genes, it could be explainable by inheritable epigenetic action on genes – “genes plus epigenetics equals destiny”

2.       Conversely, it suggests that things that have been ascribed to genes may be explained by epigenetics happening right now – a group’s intelligence may be improved or decreased right now by moving to a different physical environment, and that improvement or decrease is inherited (vaguely similar to an episode of the original Star Trek TV series where exposure to mine air lowered intelligence and increased aggression).

The Rich Get Richer, the Poor Get Poorer

However, when I look at the research findings up to now as presented in “The Embodied Mind”, it is apparent that the picture is much more one-sided than it first seems.

Specifically, every research finding cited is of an inherited epigenetic trait that is triggered, more or less, by the physical environment, and applies to all those who are affected by that physical environment state, no matter what their genetic differences are.  Let me restate that:  no matter what group (including male or female) I belong to, I am equally susceptible to proneness to obesity and related disorders if my mother or grandmother underwent prolonged starvation compared to anyone in any other group.  If my mother smoked or drank during pregnancy not only she but I will be at increased risk for cancers or alcoholism – because those gene expressions are epigenetically transmitted to the fetus.  Of course, in the last case one can argue that my “culture” made my mother more or less likely to smoke or drink; but (a) that’s something that can be mitigated by changing education and social encouragement, and (b) in most “races” or ethnicities this is not thought of as part of the core culture.  Anyway, these are just two examples:  in all other cases cited in “The Embodied Mind”, there is no inherited differentiation based on society at all, and therefore no role for race or ethnicity in causing differences.

I must point out that it makes sense that it be so.  It is logical that if 99% of our genes are identical, epigenetics should apply equally to genes that are otherwise the same and genes that are different across individuals and groups.  Therefore, when epigenetics is involved, it makes sense that 99% of the time, it is the physical environment within the last 1-3 generations that is my destiny, and that I can very possibly change that destiny by changing my physical environment, just as I can change things for the better if I change my individual behavior by changing my “culture” or social environment.  

The other “theme” of recent epigenetic research is that in many cases, it involves epigenetic switch-flipping in response to an unusually stressful environment.  Thus, starvation during or near pregnancy is typically happening in response to lack of food affecting not only oneself but one’s relatives or group.  And that, in turn, often tends to line up neatly with whether the group is rich/powerful or poor/powerless.  We might expect therefore that an increasing number of the poor of any race or ethnicity who is subjected to this kind of shock will be at increased risk of diseases and disorders that affect average intelligence as measured by standardized tests, to be less likely to have the education that a rich person does, and to be less effective at jobs, all else being equal.  Likewise, the animal trained to solve certain puzzles may transmit the memory of solving these puzzles epigenetically, and therefore looks like a genetically superior animal in terms of intelligence, and yet, give those same tests to the “poor” animal and his or her descendants will become equally intelligent.

I summarize these two trends in epigenetic research as:  The rich get richer, and the poor get poorer.  Given an initial epigenetic boost, the descendants of the rich and powerful are increasingly more likely to keep getting richer, as epigenetic inheritance combines with the social-environment and educational effects of being around other well-off people, while the poor’s descendants may very well become poorer, as inherited epigenetics leads to less ability to take advantage of education, while the social environment dominated by the powerful rich reduces both access to education and job opportunities.  And yet, epigenetic research also suggests that these trends are reversible, to the point of epigenetic equality between rich and poor.

Interestingly, epigenetics calls into question the seemingly strongest research studies indicating a role of genetics in things like intelligence and job success. Take, for example, the study that found that twins in which one of the two was placed with a different family to grow up in tended to reflect their birth parents’ rather than their childhood parents’ testing success.  It seemed like an obvious case of genetic differentiation causing this result (if we assume that the placements were not causing a child of a rich/educated or poor parent to move to a physical/social environment in which the child was given different treatment because of its background).  However, epigenetics suggests that it is far more likely the difference was because of inherited epigenetic differentiation which could be reversed either by changing the physical/social environment for this generation or by “breeding the differentiation out”.

Getting Back to That Possible Death of Race …

So to explain why I think the research trend is to undercut the view of individual differences being due to group differences by race or even by ethnicity, I want to start with what the model of “evolution” of differences seems to be turning into.

As I see it, adding epigenetics to the picture leads to a model something like this:  the five causative factors of these differences seem to be genes (inherited), epigenetics (inherited), the physical environment, the social environment (culture, society, typically corresponding to ethnic or cultural differences), and individual variation not caused by any other factor.  The physical environment may also cause genetic and epigenetic inherited differences, in the case of genetics over thousands of years of time, in the case of epigenetics immediately.

The key question then becomes, how much of these inherited differences can be explained by genetic differences correlated with physical appearance or such genetically inherited traits as lactose tolerance, and how much by epigenetics?  The most likely answer, it appears, is 90-99.5% explained by epigenetics, because if we assume 50% of those times when we thought genes were to blame it was really epigenetics, then for the other 99% of the genes the differences are definitely due to epigenetics and hence if any gene is equally likely to be affected by epigenetics you get 99% x 1 + 1% x 0.5 = 99.5% of the effects of inherited differences explained by epigenetics.

But race and notions of other group-inherited “permanent” characteristics are inherently dependent on genetic evolution for their validity.  If inherited differences are based on the physical environment 1-3 generations back and are easily reversible by a different physical environment or cross-breeding, then very little of “racial” or even “ethnic” differences is explainable by genetic or even epigenetic “destiny”.  It’s easy visually to class people by physical characteristics; but it now appears that inherited groupings that do anything more than that – possibly even in the area of physical skills – will be wrong, at least 9 times out of 10.

What does that leave us with, as a guide to action?  In broad strokes, the levers available to pull to make things better have to do increasingly with the physical environment – different exposures to disease, pollution, starvation from poverty, for example.  If we take the notion of the rich getting richer and the poor getting poorer from epigenetics or the physical and social environment seriously, we should primarily favor policies that narrow the gap between rich and poor, because other research suggests that that type of move toward “equality” will lead to a better economy and greater innovation that drives life improvements of the future.  So the levers that involve making the physical environment more “equal” in specific ways sound like one place to start. 

I would also note that tackling group social inequities seems to me to be a slightly better bet to pursue than before epigenetics arrived on the scene.  Whatever the apparent split between nature and nurture before epigenetics arrived, it seems clear that social inequities affect some differentiation between groups, and more so now that those inequities can travel down to future generations via both society and epigenetic inheritance – and that such epigenetics-exacerbated social inequities can be reversed both societally and epigenetically.

I’ll add one final thought.  I haven’t touched on the whole notion of individual differentiation across groups, inherited or not.  I really don’t think there’s enough research in the area.  Still, I’ve seen enough anecdotal evidence to form the following generalization:

Groups are more similar than you think; individuals within groups are more different than you think.

That is, there are more men who wouldn’t mind donning a tutu and doing classical ballet than you think; there are more women who wouldn’t mind being bricklayers than you think; there are more white folks who like Afro-pop than you think; there are more African-Americans who like classical music than you think; on and on.

As I say, there is little research supporting this.  Still, I think it’s a useful thing to remind oneself of, whatever the passionate issue to which it applies.

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.