By Anthony Hilton | 3 Comments | 
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A Letter from a Grandfather to his Genes, Part 2
Read Part 1 here.
3. Why aren’t the nearly 100 percent of our genes that everyone shares more important than those few that vary?
Indeed, around 99.9 percent of all the genes that a human being carries can be found in all other humans, and 98 percent in chimpanzees. Similar percentages of shared genes are found in most other animal species. So obviously it’s the tiny handful of remaining genes (perhaps 30 or so out of 30,000), each of which can have different versions (alleles), that cause people, primates, and other animals to differ from each other. It is those genes that can and do differ which are the basis for an increase in altruism as biological relatedness increases. Perhaps this is the basis for the oft-repeated phrase from Freud, the “narcissism of small differences.”
Suppose that a mutation (a new allele) happens to be useful. It makes sense (from the point of view of the whole package of genes within which the mutation is immersed) that there be some way to keep it from being lost to posterity. How? Well, surely not by worrying solely or mostly about the 99.9 percent of genes all humans share. No, you have to give proper attention to that new allele. The person carrying it has to reproduce it by making babies with his or her spouse. And while some animals can just walk away at this point, leaving offspring to their own devices, humans take care of their kids, e.g., that child now carrying the good mutation. That mutation might be one that encourages a parent to take better care of her child—who may, in turn, be carrying the same good mutation. That’s the feedback loop enabling altruism in the first place.
All this requires being able to recognize one’s kids. How? There are many possible ways: Look at whose body they came out of and who had sex with the mother, or physical resemblance, or what people say about the child’s ancestry, etc. Some of these clues are more reliable than others hence the attention to “small differences.” Then the parents have to be motivated to take care of their child—who is carrying half of each parent’s genes (since mammals undergo sexual and not asexual reproduction, or cloning). For all of this to happen reliably, via accurate detection of whose child is whose, plus a desire to take care of one’s own child (rather than any child or any object in the neighborhood), there have to be genes which program us to do the right thing. Notice that if one had a desire to take care of someone else’s child rather than one’s own, that would be the end of one’s own genes—including that lovely mutation. One doesn’t have to know about genes, but one has to have the right genes in order to do the right thing for this object (child) that came out of the mother’s body and the father’s sperm. Other objects come out of our body that we certainly do not take care of (no offense intended). So what’s the difference? Genes. Genes that program the “instincts” which enable us to identify and take care of our children properly (along with what we’ve learned from our parents). And since our children have inherited those genes, 50 percent of them in each child, the genes will be self-perpetuating. Get rid of those genes for “caring-for-own-kids” and the self-perpetuation evaporates.
Now then, if that logic works so well for one’s own children, couldn’t it work, in principle at least, in regard to individuals who didn’t come out of our own bodies but who nevertheless are carrying many of our genes because we have ancestors in common that came out of the same bodies? Providing, that is, that we can identify them and then want to promote their survival and reproductive careers. Apparently we have such propensities. And that must be the basis for whatever extra cohesion we find among extended relatives compared to nonrelatives. How do you feel about your own brothers and sisters? Your nieces, nephews, uncles, aunts, cousins? Some people find themselves alienated from even their closest relatives, but that is usually because of something extremely unpleasant that happened (e.g., excessive sibling rivalry). Were it not for that unfortunate matter, surely they would not be so seemingly indifferent to them. Notice what transpires when long lost relatives suddenly find each other after decades of separation due to war, adoption, or exile. Very touching, no? All because they share genes. What alternative is there? Remember, if genes were not running the show, you wouldn’t likely have the same show repeated across every other culture. Rather, just by chance you would expect a few different shows: such as cultures in which people routinely prefer non-kin and foreigners to their own kin, where they routinely prefer to raise other ethnies’ children and give their own away to foreigners (if they have them at all). But think natural selection: Whose kids, on average, are most likely to be best off and most likely to reproduce?
Frank Salter, whose book on nationalism is strongly recommended here, uses the phrase “genetic interests” in conceptualizing the relationship between genes and their reproduction. He doesn’t mean that genes or most animals carrying genes are capable of imagining their genes’ interests, even if they act as if they could. Genes just program their carriers to act that way. Such interests are more analogous to financial interests a person might have without being aware of them, an educational fund, say, that one day a child will inherit. A rock doesn’t have an interest one way or another in remaining intact or in becoming crushed rock. But that’s because it lacks any semblance of a process dedicated to even self-interest, never mind reproduction.
It’s an empirical question how and if a human being will go about promoting his genetic interests. Just because an Icelander’s genes are heavily represented in other Icelanders and, metaphorically, have an interest in being reproduced, does not mean that they, their carrier, or anyone else will have the necessary psychological motive for, or psychological interest in, reproducing them. He might or he might not. Is there any point in saying to a reluctant Icelander, “Hey, your genes have an interest in getting reproduced, so get busy and do the right thing”? It might be worth bringing up the subject in case he had the right motives but had merely been distracted, or didn’t realize he had so many virtual brothers on the island. (Incidentally, Salter, citing recent DNA data, is confident that Europeans in general are much more closely related to each other than heretofore imagined, thanks to the small size of their early prehistoric breeding pool following initial migrations to Europe. Imagine the thousands of present-day Icelanders growing to a hundred million or so. If additional immigration were restrained, they would find themselves with millions of virtual siblings.) However, if our Icelander friend is not at all interested in those previously unimagined relatives, there may not be any point in haranguing him. If he were nationalistic, though, the fact that his genes are scattered among other Icelanders would make it all understandable; that is i.e., it would make sense that he had an evolved mechanism for acting as if he knew that they, too, were carriers of his own genes—just as a mother bird acts as if she knew that her eggs carried her genes. Look at a bird for the first time, and for all you know she may be a one-off creature that just came into the world and is unique. But if she has eggs and takes care of them and if you know all about DNA and genes, you say to yourself, Aha! She very likely has some sort of built-in, preprogrammed brain mechanisms for getting her to do all that—sitting on eggs, feeding chicks after they hatch, etc. So now when we see Icelanders or the Irish acting nationalistically, we know about the genes they share, and so it makes sense to us that they should be nationalistic—rather than, say, run off en masse to volunteer to be slaves for Africans. A few Irish are not at all nationalistic, but there are probably a few birds now and then that don’t sit on their eggs properly. No machinery is totally impervious to malfunction. And the many interesting things to do in life and the many wonderful people in other cultures can easily distract humans. One could distract a bird from sitting on her eggs.
4. Why is kinship “relative”?
If the above account of kinship is true, it means that who we consider to be “our people” will normally depend on whom we actually are most closely related to and on our ability to reliably detect who those relatives are. But “most closely” is a relative concept. How close is “close” depends on whom we are comparing, which often means whom we are competing with. Compared to chimpanzees, Africans are “closer” to Icelanders. Compared to Africans, Swedes are closer to Icelanders. Compared to Swedes, other Icelanders are closer. Our identical twin is closer than our ordinary sibling. So there are no absolutes here. But the logic implies obvious priorities. Whom we consider “our people” and ally ourselves with in a crunch will follow that logic, other things being equal. It will depend on context and on whom, if anyone, we find ourselves competing against. Confusion here is the reason for arguments over whether one should identify oneself as a “white” or as a “Englishman” or “Spaniard”.
As a practical matter, the idea of ethnic relativity may have something to do with the notion of “subsidiarity” discussed frequently by Europeans (especially the British, and especially the British magazine The Economist) in connection with the European Union. This is the idea that all problems in life should be dealt with initially at the lowest possible political level (family, or neighborhood, or municipality, etc.), and that only if insoluble at that level should they be moved to the next higher level, and finally even to Brussels and the European Union—or to the United Nations. Subsidiarity would seem to follow a general logic of human concern. The first interest of any human is normally his own welfare and future, followed by his family and up through his extended family and ethny, extending eventually to all human beings and finally to the continued existence of life in general on the planet. At the higher levels of subsidiarity, we find a universal nationalist’s respect for ethnic and cultural diversity—in contrast to homogenizing globalization.
5. Doesn’t nationalism promote wars between ethnies?
Of course. Not a problem if you love the excitement and fulfillment of warfare, and the booty. Indeed, the genetics of kinship do partly account for the wars that occur between different peoples. Race wars (big genetic differences) may come to mind as especially horrible. However, frequency of warfare has recently been reported to be positively [sic] related to genetic similarity, even after controlling for geographic proximity. Reason suggested: genetic similar means similar economic and other interests that can more easily conflict. E.g, Palestinian Jews and Arabs (genetically similar) both feel entitlement to the same land. Nevertheless, expect even closer kinship within than between such groups if they are endogamous.
But suppose you aren’t a war lover? Then go for the “reciprocity” mentioned earlier. And yes, there is a biological underpinning to it all. If that draws a blank, here’s a brief intro.
Genes can be promoted not only by squashing your competitors but also by mutual aid arrangements—between individuals who don’t necessarily share any genes at all. Think of bees pollinating flowers and getting nectar in return; or the tiny fish that nourish themselves by helpfully cleaning the teeth and gills of very large fish in coastal waters. The only way these mutually beneficial arrangements can work, long term, is by ensuring that it’s a two-way street. It can work between nearly any organisms if their mutual benefit is simultaneous, so that if either one ceases to benefit, the other automatically gets cut off, too, and so neither can exploit the other. But humans are capable of reciprocity over time. You help me today and I will, in return, help you tomorrow, thanks to our big brains that can minimize exploitation. It’s division of labor, the economists’ “law of comparative advantage,” It may account for an enormous amount of human sociality, including warm friendships across ethnic and racial lines as well as more prosaic sorts of trade and commerce. Some people’s careers make them exceptionally prone to this type of interethnic relation, e.g., academics, political and professional elites; those involved in trade and the transport of goods and people between countries, etc.
Much of our emotional make-up (genetically evolved machinery in the brain) is thought to be devoted to monitoring and regulating these reciprocities. Feelings of friendship, attachment, obligation, or guilt toward nonrelatives exist because the capacity to feel these emotional incentives promotes beneficial reciprocity. The outrage felt when we are cheated motivates us to stop giving anything to those who don’t reciprocate. Vengeful feelings motivate us to punish those who cheat on us or betray us. Specialized cognitive systems serve us in detecting cheaters. Since all humans seem to be prone to self-interested bias, cheating requires constant management. Reciprocity may have originated in relations with relatively close kin, gradually becoming extended to genetically more and more distant humans as natural selection rewarded such commerce.
Read Part 3 here.
Anthony Hilton
Anthony Hilton is Associate Professor of Psychology (Ret.) at Concordia University, Montréal, Québec, Canada.
“Indeed, around 99.9 percent of all the genes that a human being carries can be found in all other humans, …”
The numbers game
17/4/07. By Rachael Brooker and Giles Newton
A map of copy number variation in the human genome shows that we are genetically more diverse than expected.
“I believe this paper will change forever the field of human genetics,” said Professor James Lupski from Baylor College of Medicine, Texas, in November 2006.
The paper he was referring to, a map of copy number variation in the human genome, showed that large pieces of DNA are often deleted or duplicated – to an extent that startled the research community. Our genome appears even more amorphous and changeable that anyone had expected.
“Until recently, scientific dogma told us that genetic similarity between two unrelated healthy individuals was about 99.9 per cent,” says Dr Charles Lee at Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts. “The 0.1 per cent of known genetic differences were primarily in the form of SNPs (single nucleotide polymorphisms) – single base-pair changes in the DNA.”
The International HapMap Project, for example, has found millions of SNPs in the genomes of 270 people from four populations: the Yoruba people of Nigeria, Japanese, Han Chinese and people of northern and western European ancestry living in Utah.
At the other end of the scale, very big changes in the genome are rare, but relatively easy to detect as they can be seen under a microscope. But what of intermediate-sized variations – deletions or duplications of pieces of DNA ranging in size from 1000 bases of DNA to tens of thousands of bases? The frequency of such structural changes to the genome, and their importance in normal human variation, was largely unknown.
The new map of these variants, produced by the Structural Genomic Variation Consortium (a collaboration between the Wellcome Trust Sanger Institute and 12 other centres) not only shows that the variants are frequent and widespread, but also indicates key roles in human diversity, health and disease.1
“One can no longer consider human traits as resulting primarily from single base-pair changes or influenced only by SNPs,” said Professor Lupski. “With all due respect to Watson and Crick, many Mendelian and complex traits, as well as sporadic diseases, may indeed result from structural variation of the genome.”
Losses and gains
Two research papers published in 2004 described commonly occurring gains and losses of DNA in the genome of apparently healthy individuals.2,3 This was a huge surprise to most geneticists. The variations did not seem to be harmful, as they appeared to be quite common in the population and were not associated with any serious disorder. But they were large enough to encompass entire genes or non-coding functional regions.
“The problem with the original studies was that they looked at only a few people, and at a relatively low resolution,” says Dr Lee, who led one of the two projects. “What we needed was a global profile of copy number variation in the human genome.”
Further hints that the human genome might contain many copy number variations came from the HapMap Project, which in 2005 found hundreds of regions where SNPs were unexpectedly absent from the genome. Originally thought to be mistakes or experimental failures, they in fact reflected ‘holes’ – people who appeared to be perfectly healthy had pieces of their genome missing.
By studying the same 270 people as used in the HapMap, the Structural Genomic Variation Consortium produced a global genome map a year later. Using microarrays – microscope slides or chips covered in thousands of spots of DNA – to scan the human genome, they found 1447 regions that varied in copy number, covering 12 per cent of the genome or 360 million bases of DNA.
This was unexpectedly large. And it hinted at even greater variation: regions smaller than 40 000 bases still could have slipped through the net. The regions are scattered all over the genome; for any chromosome, 6–19 per cent of the DNA can vary in copy number. As Dr Lee puts it: “We’re a patchwork of gains and losses of DNA.”
“We find deletions and duplications of whole genes, parts of genes, and changes in copy number that don’t involve any genes at all,” says Dr Matthew Hurles from the Wellcome Trust Sanger Institute. “Out of 2000 well-characterised genes known to be mutated in genetic disease, 285 vary in copy number in the 270 individuals we looked at.”
Some variants picked up by the study were already known to be linked with disease. For example, the researchers expected to find deletions associated with spinal muscular atrophy and nephronophthisis (a childhood kidney disease), as their frequency in the population is relatively high. Conversely, variations that cause disease when only one chromosome is altered – such as the duplication of the PMP22 gene that causes Charcot–Marie–Tooth disease type 1a, the most common inherited neurological disorder – would not be found, as the study was looking at apparently healthy people.
But there were many new variants revealed by the study, associated with genes linked to schizophrenia (DISC1), psoriasis (PSOR1), atherosclerosis and coronary heart disease (LPA), and congenital cataracts (beta-crystallin), to name just a few. “These diseases have nothing in common except the genetic variation involved,” says Dr Hurles. “They will all need further investigation.”
Comparing the frequencies of variants in the four HapMap populations also threw up some intriguing differences, hinting at how the populations have adapted to their specific environments. The CCL3L1 gene, for example, is present in anywhere between one and 14 copies on a chromosome, and the study found that Africans carry the largest numbers of copies of the gene and Europeans the fewest (east Asians are in between). Although people with more copies have increased protection against HIV infection and disease progression, the virus is unlikely to have caused the regional disparity. As HIV has only been around for 50 years, and this change in frequency would have taken many generations, there is possibly some other selection that drove this change.
Variable outcome
The genome may be full of variants – whether SNPs or copy number variants – but how might they affect human biology? Do they, for example, affect gene activity, crucial for many functions of the cell? For a subset of human genes it appears that they do: a study of more than 14 000 genes has found that SNP and copy number variation correlated with altered gene activity in almost 900 and 240 genes, respectively.4 Surprisingly, only about 10 per cent of the gene activity variants associated with a copy number variant were also associated with a SNP.
Such findings hint that copy number variants may contribute to human diversity far more extensively than anticipated. And there may be many more, slightly smaller such variants still to be found in the genome: the current systems struggle to find variants smaller than 5000 bases of DNA, so the 1500 or so found so far could be just the tip of the iceberg.
Genetically, we are far more unique from one another than we previously thought,” says DR Lee. “Which is gratifying in a way.”
Diagnosing defects
A map of copy number variation in the human genome is not just a boon to researchers investigating the role of genes in disease, argues Dr Nigel Carter at the Wellcome Trust Sanger Institute: it can help doctors trying to find out why some babies are born with significant birth defects or go on to have severe learning difficulties. “About 2–3 per cent of babies are born with such problems,” he says. “About half of these are thought to have a genetic origin, but most remain undiagnosed because when you look at the chromosomes under the microscope, they look normal.”
“Array technology is like a molecular microscope; you can go deeper into the genome to look for gains or losses of DNA. The problem then is telling which gains or losses are associated with the syndrome, but by superimposing the copy number variation profile from a patient onto the map from normal individuals, you can see which gains or losses are normal variants, and which are associated with a syndrome.”
The Wellcome Trust Sanger Institute has set up a database called DECIPHER, and is encouraging clinicians around the world to use the database to help to interpret genome changes found in their own patients. Over 60 clinical centres around the world are currently contributing cases to the database, which grows daily.
Rachel Brooker is a research associate at the University of Newcastle and Giles Newton is Senior Science Editor at the Wellcome Trust.
References
1 Redon R et al. Global variation in copy number in the human genome. Nature 2006;444(7118):444–54. Abstract
2 Sebat J et al. Large-scale copy number polymorphism in the human genome. Science 2004;305(5683):525–8. Abstract
3 Iafrate AJ et al. Detection of large-scale variation in the human genome. Nat Genet 2004;36(9):949–51. Abstract
4 Stranger BE et al. Relative impact of nucleotide and copy number variation on gene expression phenotypes. Science 2007;315(5813):848–53. Abstract
One thing we need to keep in mind with humans is that we are capable of seeing our OWN patterns over time, and therefore perfecting and directing the otherwise blind and mindless pattern of biological urges other organisms are ruled by. We see high destinies in certain behaviors, and no destiny or only destruction in others — even saying “there is no future in that” about certain patterns like crime.. or “the wages of sin is death”. This is why race-mixing is a definite sin (eventual corruption and destruction / death, i.e. no future in it) and should be classified with other immoralities and legislated against. We have a certain pattern as Europeans which would be snuffed out by other ways and patterns — they are incompatible. I know we are not supposed to say this, but ours IS a superior pattern objectively. We can overcome more environmental obstacles and survive into the farther future with objective science rather than just strategic violence or just complex hierarchical social structure or etc. Accurate INFORMATION should be the recognized measure of evolution, morality, and survival. Lies and liars are especially bad and immoral to OUR ways..
You could make a great case that all religion was founded and started by this higher ability to recognize larger eternal patterns in us — basically as an Eugenic mechanism seen “through a glass darkly” in the past… eschewing animal passions and trying for a higher destiny. It is no accident that a religious monk discovered genetics (Mendel). Religion IS eugenics… Morality IS eugenics… yet one group with other biological patterns (hint: it starts with a “J” and ends with “eww”) and destiny at odds with us says that eugenics is somehow “immoral”?!? That is only because they wish to get rid of us, and our higher destiny before we realize it and they are unable to compete. Hyenas sneak around to eat lion cubs voraciously when they can for the same reason. See my book: “The Textbook of the Universe: The Genetic Ascent to God” for more on this perspective.
Addition: Notice how in the article they had to select and put into it a mention of genes which show African “superiority” and European “inferiority.” Such a subconscious propaganda has become normal part of science articles related to humans.
Re: Romer
My friendly advice.
Let me first say to you that caring about genetic continuity is a good and necessary thing. That said, your writings sound a bit extreme. Your knowledge about genetics is likely to be accurate, but it might have become so at the expense of other things in life. Genetics is embedded in larger context in life; it can’t float alone in some supreme abstract information space. If genetics becomes a narrow and exclusive way of observing the world, it can produce such overconfident and pseudoreligious goals as “The Genetic Ascent to God,” and claims that the general Jewish way of looking at the world is a genetic attack. If and when Jewish and other liberals produce genetic discontinuity, it is because of multiple and complex reasons, many of them mundane, small, ignorant, stupid, self-destructive, and/or pathetic.
You could expand your knowledge with social psychology, political philosophy, and studies about enduring successful communities.
I leave you to contemplate this: Although science has naturally become fragmented into many parts because of the limits of human capacities and time, it has been incorporated into the liberal governmentality as a method of control. As long as the scientists and others have only a narrow specialized knowledge, those with the largest overview together with certain key specialized knowledge rule the system.