More Defense of the EGI Concept

More on Salterism.

Some critics of so-called “Salterism” and critics of me for defending the EGI concept (Lawrence of Alternative Right as one example) get offended when I mock their (repeatedly refuted) “critiques” and state that the EGI concept is “self-evident.”  That last part really seems to annoy them. But to understand why I say that let’s simply look at the basic premises underlying EGI. These are premises that any honest person, with an objective understanding of genetics, race, and evolutionary biology, must agree with. While we can understand mendacious race-denying leftists screeching incoherently against “racist” facts, one would assume that the allegedly more “race realist” Right would have no problem with the following:

• 1. There are genetic differences between population groups.
• 2. Members of these groups (at least at the racial level and in many, likely most, cases at lower levels as well) are more genetically similar to members of their own group than to other groups (this obvious fact was formally demonstrated at least by the year 2007).
• 3. According to evolutionary biology and the generally accepted neo-Darwinian understanding, it is adaptive to promote the interests of those more genetically similar to you than those more distant. Even academics like Brigandt – trotted out by anti-EGI HBDers in an attempt to refute ethnic nepotism – agree with this general premise.  Apart from hardcore ideological crazies, this really isn’t up for debate any more.
• 4. The concept of genetic relatedness and the pursuit of adaptive fitness (inclusive fitness) is context dependent. Thus, if the entire world was composed of just one ethnic group, there would be no ethnic genetic interests per se (since there is a common ethnic genetic background), but there would be personal and familial genetic interests, as some people within this population are more closely related than others (e.g., family kin).  But in a world of different and competing ethnic and racial groups, in the context of making choices between co-ethnics and others, there are ethnic genetic interests based on the genetic differences between groups (multiplied by their large numbers). Of course, in the latter scenario, personal and familial interests still count, but given ethnic conflict, higher level ethnic interests often must be prioritized. Also, the ever-inventive critics of EGI always come up with fanciful, unrealistic scenarios in which they claim adherence to EGI would not be adaptive. That approach is ludicrous because one can invent any number of bizarre scenarios to invalidate just about any normative behavior. Rational people deal with rules that apply to real-life scenarios that constitute some of the most serious problems of our time, including ethnic conflict and race replacement. Grasping frauds waste time trying to distract us from reality.

I say that EGI is self-evident because it is self-evident.  One can expect the crazed Left – that tells us that there are no differences between Europeans, Africans, and Asians, but that Europeans are uniquely evil and must be replaced – would reject the premises listed above. But the Right?

EGI is truth. That doesn’t change just because you endlessly cite HBD talking points that have been repeatedly refuted for the past twenty years. It also doesn’t change because you repeatedly quote, completely out of context, a single sentence from Salter’s On Genetic Interests. Those behaviors just make you look like a moronic contrarian, a retarded buffoon.

Some links to my various defenses of the EGI concept (“Salterism”) can be found here. Rather than repeat any of that, I’ll link to this piece by Salter. With respect to the free rider objection:

…members of bands and tribes can behave altruistically without being selected out by free riders. Eibl-Eibesfeldt (1982) argued from his field observations that mutual monitoring, ubiquitous in small-scale societies, is sufficient to suppress cheating. He pointed to the pronounced group identity and mutual support found in primitive societies, and argued that this originated in kinship bonds. The cohesion of band and tribal societies makes them units of selection, Eibl argued. This point was elaborated by Boyd and Richerson (1992), who argue that monitoring and punishment are so effective in small scale societies that they allow the evolution of cooperation, or any other characteristic that is promoted by a culturally-governed group strategy.

Whether or not one accept that group selection has figured in human evolution, the mechanisms advanced by group selectionists are sufficient to allow a more conservative process, extended kin selection, to occur. In fact this is what Eibl has always meant by his version of group selection.

A final mechanism deserving of mention is collective goods. A criticism of extended kin selection is that it is impossible for an individual effectively to invest in a kin group much larger than a family, because the benefit would be spread so thinly that the payoff would always be greater from investing in close kin, rather than distant ones. Goetze (1998) has dispelled this concern. He draws on economic theory to argue that by contributing to collective goods—such as hunting large game animals or defending the group—allows an individual to confer a large fitness benefit on a large number of individuals.

So there is no mechanical problem with the feasibility of individuals showing altruism to kin groups larger than the extended family. Indeed, all these mechanism—control of free-riders, bonding the group, and choosing or fashioning collective goods—are highly scalable. They can be increased in scale to accommodate a kin group of any size.

See here for a published analysis, using computer simulations, demonstrating the dominance of ethnocentric behavior over free riding and “humanitarianism.” Salter is of course correct, and his critics wrong. The evidence supporting EGI is so strong, and is repeated throughout so many different domains of analysis, that I believe I am justified is terming the concept self-evident.  I am also justified in ascribing either mendacity or stupidity to its critics.

With respect to inclusive fitness extending beyond the family into ethnic kin and moving beyond simple genealogical identity by descent to identity by state (that is a deeper level of identity by descent, after all, at least when talking about ethny) with respect to genetic similarity, see this from Salter:

The point that inclusive fitness processes can operate between individuals merely on the basis of genetic similarity, without any genealogical information, is critical, and I quote Hamilton’s commentary on this theoretical advance.

“Because of the way it was first explained [by Hamilton], the approach using inclusive fitness has often been identified with “kin selection” and presented strictly as an alternative to “group selection” as a way of establishing altruistic social behaviour by natural selection. But…kinship should be considered just one way of getting positive regression of genotype in the recipient, and that it is this positive regression that is vitally necessary for altruism. Thus the inclusive fitness concept is more general than “kin selection” ” (Hamilton 1975, pp. 140-41; [p. 337 in the 1996 reprint]).

This frees the analyst from the “identical by descent” clause in Hamilton’s original (1964) formulation, allowing the direct measurement of kinship processes using genetic assay data…

In response to HBD-inspired lies that kinship is not significant past immediate family, and is irrelevant to ethny, here is Harpending's paper describing the basic fundamentals Salter used (with Harpending's assistance) in On Genetic Interests.

The coefficient of kinship between two diploid organisms describes their overall genetic similarity to each other relative to some base population. For example, kinship between parent and offspring of 1/4 describes gene sharing in excess of random sharing in a random mating population. In a subdivided population the statistic Fst describes gene sharing within subdivisions in the same way. Since Fst among human populations on a world scale is reliably 10 to 15%, kinship between two individuals of the same human population is equivalent to kinship between grandparent and grandchild or between half siblings. The widespread assertion that this is small and insignificant should be reexamined.

Now, with respect to Brigandt-like arguments about “the evolution of…XYZ” I have stated many times that EGI is a rational prescriptive argument has no need for the “evolution” of anything – general domain behavior can be applied to pursuing ethnic interests (genetic or otherwise).  Just as humans did not have to evolve a specific ability to use a computer but rather just evolved the cognitive and behavioral traits that make such use possible, nor is it necessary to evolve specific behaviors to pursue particular approaches to the pursuit of personal and group interests.  Having said that, any reasonable look at human history does support the idea of a descriptive validity of EGI to a considerable extent, particularly when we understand that various proxies for genetic relatedness (e.g., national identity and loyalty) have been used to mobilize human behavior. Salter writes:

Thus the second problem in understand the evolution of ethnocentrism the second is already solved, or well on its way to being solved. It’s the first problem that remains; indeed, it has hardly been addressed. To reiterate, was the kinship between random members of bands and tribes large enough for altruism directed between them to have been adaptive?

Since, as stated, I don’t believe that the “evolution of…” argument has merit, I won’t reproduce any more of Salter’s riposte here; you can read what he wrote in the original article as well as, of course, in On Genetic Interests.

It is clear then that the EGI concept has survived repeated attempts at refutation. Again, the description of self-evident seems valid. Why then the opposition?  Well, it is quite clear why the Left would oppose the idea, people who deny the existence of race, who obfuscate genetic differences between groups, who object to Whites defending their group interests, and who promote an EGI-destroying multiracialism for White nations, will of course object to any paradigm that stands against their most fervent desires and most fundamental objectives. EGI is a threat to the entire globalist, multicultural experiment. But what about the Right?  Certainly, we can understand that the civic nationalists will also object to anything that disrupts the fictional “identity” of a multiracial nation and that stands against aracial constitutional patriotism. The religious Right tell us that all people are “children are God” and thus they would reject EGI for that reason. The Right is also anti-science, so that influences negative attitudes to EGI.  The Far Right has been infected by the HBD virus, so let’s look at why HBD opposes EGI and thus dissolves the natural affinity one would assume pro-White activists would have for EGI.

The idea that HBDers oppose Salterism because they sincerely believe it is wrong can be dismissed based on what is written above. HBDers may be mendacious, they may be evil, but they are not stupid. Obviously, they must know Salter is correct. When their own poster boy for opposition to ethnic nepotism – Brigandt – admitted in writing that favoring ethnic kin is adaptive (the essence of EGI), then, really, the mask is torn off. That leaves us to consider their motivation for lying to their followers by attacking an idea that they know is correct. 

The most charitable explanation is that they believe that their alternative view of society – aracial cognitive elitism – is the best option and they are willing to do anything, including engaging in the most outrageous fundamental dishonesty, in order to achieve their dream of “IQ nationalism” where “high IQ” Jews, Asians, and Whites (and whatever intelligent fractions of other groups) live in “Jeurasian” harmony.” A less charitable, but more realistic, interpretation is that HBD is a political movement of naked ethnic and personal self-interest by Jews, Asians, and Whites who have thrown in their lot with Jews and Asians for various reasons (intermarriage, “race realist” ideology, aesthetic preferences, or simply being traitors who help the enemy in exchange for something). Thus, the objective is a society dominated by “high IQ” Jews and Asians, with subaltern Whites as helots and a mixed-race Jeurasian managerial elite between the upper and lower strata of this “cognitive elitist” society. In essence, they want a society modeled after the family of a certain race-mixing White HBDer – ethnocentric Asians (and Jews) in charge, Whites engaging in “measured groveling” to their overlords, and Whites losing their racial integrity through “Jeuraisan” admixture, with of course Asians maintaining their racial integrity in their homogeneous homelands and a core of Jew maintaining themselves, in both Israel and in the Diaspora. Further, individuals (including Negroes – even though Negroes are typically denigrated by HBD) who have an agenda specifically against White nationalism, particularly the pan-European variety of White nationalism, will strategically support HBD in order to prevent the rise of “Whites only” kinship-based movements. 

Something else needs to be said. The same buffoons on the Right (Lawrence, for example) who attack EGI also attack MacDonald's term "group evolutionary strategies." That's interesting because the HBDers also attack that idea as well as EGI. Those with long memories recall Derbyshire's hit piece on MacDonald where Derbyshire mocked the idea of what a group evolutionary strategy is. After all, why would a White HBDer, married to a Chinese woman, and with half-Chinese children, have a problem with racial groups (like Whites and Asians, for example) being in competition, each with their own group evolutionary strategy?  A mystery it all is!  Just like it is a mystery why the South Asians of GNXP, and their White fellow travelers, would oppose the idea of Salter's EGI. All very mysterious indeed! Equally mysterious is why an ostensibly pro-White individual would follow the lead of transparently self-interested HBDers.

What about the potential accusation that I'm engaging in a logical fallacy by questioning the motivations of my opponents rather than engaging their ideas?  That is laughably false since I have been engaging with those ideas for the past twenty years, writing one long treatise after another defending EGI and group evolutionary strategies, and thoroughly refuting the criticisms of those paradigms. I think that after two decades of "engaging with their ideas" I'm now entitled to speculate on the motivations of those that continue to peddle the same nonsense (and for the most part refuse to engage with my ideas, by the way).

It should be obvious, however, that whatever the motivation of the HBDers, their anti-White ideology and agenda should be unalterably opposed by those who claim to be pro-White nationalists of one sort or another. That much of the “movement” supports HBD, and attacks EGI, clearly demonstrates how intellectually, politically, morally and spiritually bankrupt the “movement” really is.

Indeed, if one was to rationally criticize EGI, one could state that it does not go far enough – the original analysis depends on “beanbag genetics” – considering genes in an atomized fashion – and neglects genetic structure and genetic integration.  I’ve written about this previously and one can find that work on this blog so I need not get into that here, beyond repeating that the basic problem with EGI is not that it is wrong, but quite the opposite – it is so right that even its originator didn’t realize the full scope of its implications.

We should not let the critics of EGI off the hook by allowing them to simply regurgitate nonsense refuted years ago or quote individual Salter sentences out of context. If they believe EGI is wrong, they need to point out which of the four premises listed above are wrong. The Left no doubt would reject points one and two, demonstrating how they dabble in pseudoscientific "woke" nonsense. Those on the Right would (I hope) accept premises one and two. That leaves rightist EGI critics to target premises three and four. But if they say premises three and four are wrong, then they must believe that (a) making no distinction between genetically similar co-ethnics and genetically distant others is adaptive, or (b) it is more adaptive to favor genetically distant others than genetically similar co-ethnics.  Which is it? These idiots need to be held to account and they need to be put on the spot and tell us if they, like the Left, reject genetic science (premises one and two), or if they reject premises three and four and instead believe in (a) or (b). It has to be one of those choices. Being a contrarian buffoon or a gullible idiot who mindlessly swallows HBD swill is not sufficient. They have to make a stand about the four premises and point out what alternatives they support if they believe that those premises are wrong.

In any case, EGI-denial is, in my opinion, on par with Flat Earth, viruses don’t exist, and other example of rank stupidity. It is also equivalent to race denial, and is actually ideologically associated with that, since a denial of a biological basis for race would lead one to reject EGI as well. I have previously written that the “movement” attitude toward Salter’s work is perhaps my biggest disappointment in all my years of activism.  After all, I always knew that Nordicism was “baked into the cake” of the “movement,” but the idea that pro-White advocates would ignore and even attack an intellectual paradigm, produced by an academic, that is both manifestly true and also provides support for pro-White politics, is simply astonishing. If one thing demonstrates the utter depraved and retarded vacuity of the “movement,” well, that is it.

Emergent Properties of Human Populations

Total is greater than the sum of the parts.

If one considers ethnic and racial differences at the population level, with respect to intelligence, behavior, and achievement, these differences often seem greater than what one would expect by comparing the averages, or the bell curve distributions, of these traits between the relevant populations.

This is somewhat analogous to comparing genetic structure between populations as opposed to a simple allele-by-allele measure of gene frequency distributions; the differences are much larger in the former than in the latter.

Thus, if one were to pick some psychometric trait and measure individuals of different populations, and plot the results, you would get bell curve distributions for each trait in which, as is likely, considerable overlap between the populations exist. And yet, looking at the populations as a whole, the result is typically a quite marked difference in the outcomes of national behavior and achievement.  This is likely due to:

1. These differences are amplified over the large numbers of people involved, and, more importantly, the interactions between people in a population creates a synergy between these peoples and their behaviors, so that the behavior of the population is an emergent property of the behavior of the individuals making up that population. One cannot then say that a population with an IQ five points higher than another population will exceed that other population only by the same degree that an individual with an IQ five points higher than another individual will outdo the performance of that other individual. At the population level, the outcome will be more marked, as many individuals of a different IQ distribution interact and create or inhibit opportunities for others in the same population.  These processes will be further amplified by mechanisms 2-5, below.

2. While there is much overlap in the bell curves, there can be significant differences at the left and right tails of the curves. So, while the averages may not differ so much, there may be larger differences among the extremes that will have an outsize influence on the outcomes of the society. One population may have many more geniuses, many more adventurers, many more inventors, many more non-conformists, many more mentally sound and stable individuals; while other populations may be "enriched" with more retards, mattoids, neurotics, insect-like conformists, etc. These extreme fractions, in synergy with the smaller mass average differences, can leverage the societal outcome to a degree much larger than would be expected from the mass average differences alone.

3. There is cross-talk feedback between the traits of a people and the culture created by these traits, so small original differences become amplified over time. Thus, we have "canalization" of peoples in certain directions, creating cultures and civilizations that are more unique than what we would expect simply looking at specific traits in isolation.

4. We must remember that the outcome is not due to any single trait, but all of the traits working together, over large numbers of people, influenced by all of the other factors mentioned. So, analogous to genetic structure, and how that structure is an emergent property of considering allele frequencies together as a group, when one considers all population traits together, the relatively small differences of each trait become more important as they interact with differences in many other traits, even if those other differences are, on their own, relatively small as well. Again, we should not consider traits in isolation.

5. Points 1-4 above affect how a people respond to various "accidents of history" - so the combination of inborn traits, culture, and historical processes make populations diverge to a much greater extent than what could be expected by the mass averages of the inborn traits themselves.

Hence, the total, the outcome, is greater than the sum of the parts, and the character of a nation is an emergent trait derived from what in theory are (in some cases) relatively small differences in mass average intelligence, ability, and behavior.

PopGen June 2019

Two papers.

The first:

Abstract

In many species a fundamental feature of genetic diversity is that genetic similarity decays with geographic distance; however, this relationship is often complex, and may vary across space and time. Methods to uncover and visualize such relationships have widespread use for analyses in molecular ecology, conservation genetics, evolutionary genetics, and human genetics. While several frameworks exist, a promising approach is to infer maps of how migration rates vary across geographic space. Such maps could, in principle, be estimated across time to reveal the full complexity of population histories. Here, we take a step in this direction: we present a method to infer maps of population sizes and migration rates associated with different time periods from a matrix of genetic similarity between every pair of individuals. Specifically, genetic similarity is measured by counting the number of long segments of haplotype sharing (also known as identity-by-descent tracts). By varying the length of these segments we obtain parameter estimates associated with different time periods. Using simulations, we show that the method can reveal time-varying migration rates and population sizes, including changes that are not detectable when using a similar method that ignores haplotypic structure. We apply the method to a dataset of contemporary European individuals (POPRES), and provide an integrated analysis of recent population structure and growth over the last ∼3,000 years in Europe.

That's interesting, I suppose, but what is really needed from population genetics is two things.  First, global assays of genetic kinship.  Second, application of genetic structure and genetic integration (e.g., Gillet and Gregorious) to human genetic data. These things are consistently not being done. Is it because they are viewed as uninteresting to the field, or is it because the findings would be politically unpalatable to the field?

Author summary

We introduce a novel statistical method to infer migration rates and population sizes across space in recent time periods. Our approach builds upon the previously developed EEMS method, which infers effective migration rates under a dense lattice. Similarly, we infer demographic parameters under a lattice and use a (Voronoi) prior to regularize parameters of the model. However, our method differs from EEMS in a few key respects. First, we use the coalescent model parameterized by migration rates and population sizes while EEMS uses a resistance model. As another key difference, our method uses haplotype data while EEMS uses the average genetic distance. A consequence of using haplotype data is that our method can separately estimate migration rates and population sizes, which in essence is done by using a recombination rate map to calibrate the decay of haplotypes over time. An additional useful feature of haplotype data is that, by varying the lengths analyzed, we can infer demography associated with different recent time periods. We call our method MAPS for estimating Migration And Population-size Surfaces. To illustrate MAPS on real data, we analyze a genome-wide SNP dataset on 2224 individuals of European ancestry.

I'm not going to judge the validity of this approach without more data; however, any cursory look at current population genetic studies illustrates how the "testing companies" are behind the cutting edge of methodology.

Largely speaking, the spatial variation in inferred dispersal rates and population densities is remarkably consistent across the different time scales (Fig 4). In the MAPS dispersal surfaces, several regions with consistently low estimated dispersal rates coincide with geographic features that would be expected to reduce gene flow, including the English Channel, Adriatic Sea and the Alps. 

In general, geographic barriers have historically impeded (but obviously not abrogated) gene flow.

In addition we see consistently high dispersal across the region between the UK and Norway, which may reflect the known genetic effects of the Viking expansion [22]. 

See more on this below.

These features are consistent with visual inspection of the raw lPSC sharing data (S4b Fig). The MAPS population density surfaces consistently show lowest density in Ireland, Switzerland, Iberia, and the southwest region of the Balkans. This is consistent with samples within each of these areas having among the highest PSC segment sharing (S4a Fig). The MAPS inferred country population sizes are also highly correlated with estimated current census population sizes from [36] and [37] (S5 Fig) which can be mainly attributed to the fact that lPSC segments are highly informative of current census population sizes (Fig 5).

And then:

We do note the lower estimated dispersal rates between Portugal and Spain compared to the rest of Europe in the analyses of longer PSC segments (5-10 and > 10cM), and the higher estimated dispersal rates through the Baltic Sea (> 10cM segments), possibly reflecting changing gene flow in these regions in recent history.

I'm not sure what to make of that Iberian data.  I'm not aware of any significant geographical barrier there, so is that an example of political barriers affecting gene flow?  The data of this paper call into question "testing companies" using generalized "Iberian" or "British/Irish" ancestral categories.

Our estimates of dispersal distances and population density from the POPRES data are among the first such estimates using a spatial model for Europe (though see [30]). The features observed in the dispersal and population density surfaces are in principle discernible by careful inspection of the numbers of shared PSC segments between pairs of countries (e.g. using average pairwise numbers of shared segments, S4b Fig, as in [20]). For example, high connectivity across the North Sea is reflected in the raw PSC calls: samples from the British Isles share a relatively high number of PSC segments with those from Sweden (S4b Fig). 

This is consistent with what is mentioned above, compatible with the historically known gene flow from Scandinavia to the British Isles, particularly England, during the Viking age.

Also the low estimated dispersal between Switzerland and Italy is consistent with Swiss samples sharing relatively few PSC segments with Italians given their close proximity (S4b Fig). 

The Alps being one of the geographical barriers mentioned above.  This of course is not compatible with Der Movement dogma of Northern Italians being "Celto-Germanic Nordics."

However, identifying interesting patterns directly from the PSC segment sharing data is not straightforward, and one goal of MAPS (and EEMS) is to produce visualizations that point to patterns in the data that suggest deviations from simple isolation by distance.

The inferred population size surfaces for the POPRES data show a general increase in sizes through time, with small fluctuations across geography; In our results, the smallest inferred population sizes are in the Balkans and Eastern Europe more generally. This is in agreement with the signal seen previously [20]; however, taken at face value, our results suggest that high PSC sharing in these regions may be due more to consistently low population densities than to historical expansions (such as the Slavic or Hunnic expansions).

Relative population density may be a driver of genetic history, and one ignored by Der Movement in lieu of more colorful stories about expansions and admixture.

Second paper:

The roles of migration, admixture and acculturation in the European transition to farming have been debated for over 100 years. Genome-wide ancient DNA studies indicate predominantly Aegean ancestry for continental Neolithic farmers, but also variable admixture with local Mesolithic hunter-gatherers. Neolithic cultures first appear in Britain circa 4000 BC, a millennium after they appeared in adjacent areas of continental Europe. The pattern and process of this delayed British Neolithic transition remain unclear. We assembled genome-wide data from 6 Mesolithic and 67 Neolithic individuals found in Britain, dating 8500-2500 BC. Our analyses reveal persistent genetic affinities between Mesolithic British and Western European hunter-gatherers. We find overwhelming support for agriculture being introduced to Britain by incoming continental farmers, with small, geographically structured levels of hunter-gatherer ancestry. Unlike other European Neolithic populations, we detect no resurgence of hunter-gatherer ancestry at any time during the Neolithic in Britain. Genetic affinities with Iberian Neolithic individuals indicate that British Neolithic people were mostly descended from Aegean farmers who followed the Mediterranean route of dispersal. We also infer considerable variation in pigmentation levels in Europe by circa 6000 BC.

Contra Duchesne, ancestry deriving from Neolithic farmers is not restricted to Southern Europe; it is just much more concentrated there.

Movement and Epimovement

Clarifications.

Read this, dated November 29, 2018

Read this, dated August 1, 2018.

Hmm…Der Movement catches up eventually.

Now, Zman’s complaints are for the most part correct (if overblown); epigenetics is being grossly over-interpreted by both the Left and the Traditionalist Right.

However, as I wrote:

While I believe that epigenetic influences are grossly overestimated by ideologues of both the Left and Right, who have political reasons for de-emphasizing genetic determinism, it is wrong to lurch in the opposite direction and completely disregard potential epigenetic mechanisms.

We cannot completely rule out epigenetic mechanisms as a secondary, reinforcing, weaker mechanism for race-culture, the primary mechanisms being genetic differences and learned culture.  By a crude analogy to physics, genetics and culture are “strong forces” (e.g., nuclear) while epigenetics is a weak force (e.g., gravity).  But gravity, while being a weak force, is somewhat relevant to someone falling off a building. When dealing with objects with large mass, like the Earth, gravity is strong in aggregate; the same could be held for weak epigenetic influences that, if present over entire populations, can exert considerable racio-cultural force.

Having said that, my work over the years makes clear that I am NOT any sort of proponent of epigenetics as a significant factor in racial differences – those differences being CLEARLY genetic in origin.  Thus, the EGI Notes post linked above spends 99% of its content discussing Gene-Culture interactions, with epigenetics as a side note. 

In summary: Epigenetics may have a small and secondary but not completely insignificant role in reinforcing certain isolated and specific characteristics that are primarily determined by the interplay of genes and culture. However, the environmental influences that possibly exert effects through epigenetics must be consistent over time if you wish the epigenetics to be equally stable.  Epigenetic effects of starvation, for example, can be passed down from parent to child but it is unlikely that this will be carried down endlessly through time…unless the Dutch are continuously subjected to famines every few decades.  So, a consistent environmental factor could in theory continuously reinforce an epigenetic modification, but a one-off event is not expected to permanently alter a people’s epigenome.  Of course, given shifting gene frequencies over time, and effects of selection, changing environments will alter a populations’ genome as well.

Another analogy may be useful here.  Imagine an important book that describes Culture.  The main content of the text, the main text, the vast bulk of the words, explanations, meanings, and arguments are the Genes. In contrast, Epigenetics would be the footnotes to that main text. Many of the footnotes would be relatively unimportant; however, several of them would be very important clarifications of the meaning of the main text. In subsequent editions of the book, one would find that the footnotes are changing more frequently (additions, deletions, modifications) than is the main text; every once in a while, a significant change in the main text happens and that would be a particularly important new edition of the book.

That, given what we know now, puts things in the proper perspective.  The Traditionalists (and the Left) are wrong to elevate epigenetics as somehow the equal (or superior!) to genetics; the HBDers are wrong to equate the reality of epigenetics to crude Lamarckianism.  Both sides are politically motivated.  Real science keeps on investigating, though – speculating, hypothesizing, testing, and evaluating

And how about this analogy – the core reality of racial and cultural differences constitute the “genetics” of racial activism; while more ephemeral phenomena – influenced by people’s agendas – such as Traditionalism or HBD are the “epigenetics” of racial activism, mere footnotes (and in those cases, not clarifying at all).

Let us now consider some “words of wisdom” – dating from the mid-late 1990s – of a well-known “movement leader’ who shall remain nameless since this was from a private conversation.

First, with respect to the situation in Russia at that time, this “leader” suggested that it would be good if the Communist Party came back into power there, since they were “anti-Jewish” and “anti-globalist.” By that logic, the Islamic takeover of Europe is a good thing, since they are also anti-Jewish and anti-globalist.

Then, in response to my suggestion that this “leader” and his group utilize stock market investment (and other financial instruments) to grow their portfolio and hence have more funds for their activism – “no, I don’t want to do that, because playing the stock market is like gambling,”

Of course, proper fund investing, starting from that time and extending 20 years (until fairly recently) would have yielded an approximate 200% increase in funds.  Other investments would have yielded a greater positive outcome.

Thus, I’m sure readers of this blog will be shocked – shocked I say! – to learn that Sallis was right and The Fearless Leader wrong.  But, hey, keep on following these leaders because….affirmative action.

Oh, for godssakes:

Lord of the Rings is now being posited as a European meta-myth that can help guide us back from the brink.

I really do suspect an ethnic element in this – the “subracial soul.”  What some of us see as tiresomely boring, juvenile, and pretentious, others see as the core around to build a “European meta-myth.”  Sorry, friend, not all Europeans are buying it, only that fraction for whom “being snug in your hobbit hole” resonates as a “Faustian drive.” Sure enough, after all, burrowing into a hole in the forest and pretending to playact as semi-feudal “traditionalist” “hobbits” is better than all that scientific mumbo jumbo about “reaching the stars” (not Faustian that!) – we’ll leave all of that science and technics stuff to the Chinese, who will of course ultimately learn that they can’t power their steampunk starships because peak oil.  But them, I’m just a crazy and bitter orc and hence to be ignored.

Those wild and crazy South Asian cognitive elitists:

…a curious anecdote he relates about his own Bengali immigrant mother. Supposedly, when challenged by another woman (presumably white) for having such a large family at a time of a “population crisis,” Salam’s mother responded that “she fully intended to have a large family so that she and her offspring would displace America’s native inhabitants, just as European settlers seized the lands of the American Indians.”

That my friends is the essence, the fundamental meaning, the underlying core, the reality of “HBD race realism” – arrogant Asians and Jews replacing Whites, dispossessing Whites, gleefully subjecting Whites.  All promoted by the likes of John “self-admitted measured groveling to my Asiatic wife” Derbyshire.  Delenda est HBD!

Roissy:

The lawlessness of the FBI, CIA, and DOJ beggar belief. I’m not kidding when I say creeps like Brennan, Comey, Clapper, Strzok, Rosenstein, and Mueller should be in the docket to answer for their crimes of treason.

So why does Trump do absolutely nothing?

Genetic Structure and Altruistic Self-Sacrifice

A more precise accounting is required.

We are all aware of Haldane’s oft-quoted assertion that he would lay down his life for two brothers or eight cousins, the genetic payoff of such altruistic self-sacrifice being the equivalence – as measured by ”bean-bag” genetics – of the numbers of gene copies between these sets of relatives.

In general, I am in broad agreement with the sentiment, although as we shall see, it requires modification.  Even more broadly, those on the Far Right invoke this paradigm to support the idea of altruistic self-sacrifice in favor of larger numbers of an ethny, in defense if ethnic genetic interests.  Likewise, I support that as well, with the proper modifications as with the smaller-scale examples of familial relatives.

Even though at first glance, Haldane’s reasoning seems sound, likely most people would be hesitant to follow that advice.  In large part, this is the natural impulse of self-preservation, but there are other reasonable objections that can be made.

One could argue, all else being equal, that judging between two sets of equivalent genetics, it’s better to preserve yourself for reasons of control.  A person concerned enough with genetic continuity that they would consider such altruistic self-sacrifice is someone likely to start a family, care for children, and properly actualize the continuity. Can you be sure your two brothers would do the same?  Why are they in the position that they need your sacrifice to begin with?  Are they stupid?  Reckless? Are you sure they’ll act in support of your (in this case indirect) genetic continuity with the same vigor you would do for yourself?  So, to be safe, maybe you need to raise the bar for self-sacrifice to three brothers or ten cousins?

A more important reason, and one that may be intuitively sensed by most people even though they wouldn’t be able to explain it, or likely even articulate their feeling about it, is that there is more about kinship than mere numbers of gene copies.  Genetic structure is important – what genes are coinherited and, to the layman’s eye, what phenotypic traits (derived from those genes) are inherited together.  Of course, family is going to be more similar here than (co-ethnic) strangers, but similarity is not identity.  Even with siblings (apart from identical twins, which are a special case), recombination and independent assortment will ensure that your brothers will have a distinct genetic stricture from you.  Now, granted, these same processed, even with a co-ethnic mate, will ensure that your children will also have a different genetic structure than you, but, all else being equal, your brothers’ children will be more unlike you, with respect to genetic structure, than your own children, as the “starting point” (you vs. your brothers) is already different. So, when genetic structure is taken into account, two brothers are not really your genetic equivalent.  Apart from an identical twin, you have no genetic equivalent, just degrees of relative similarity and difference, even after numbers of gene copies are accounted for.  Then how many brothers are sufficient for self-sacrifice?  This requires a more rigorous analysis, which will be dependent upon accurate measures of genetic structure, and that’s not something we can expect SJW population geneticists are likely to do. However, while the overall Haldane argument – and its Salterian extension – makes sense the numbers given based on “bean bag” genetics is going to be an underestimation of where you need to draw the line in sacrificing yourself for others.  On the other hand, the reverse is true – if you have to choose between your brothers and strangers, or between co-ethnics and non-ethnics, taking genetic structure into account means that helping your brothers and your co-ethnics is even more important than before, because in comparison to more genetically alien peoples, genetic structure amplifies how much more close you are to your brothers and your co-ethnics.  It’s a double-edged sword: it makes your own preservation a bit more important, but it also makes the preservation of those more similar to you more important than those more distant.

Now, one can argue that after several generations of recombination and independent assortment – even assuming endogamous mating within the ethny – genetic structures derived from your posterity and those of your brothers will be more or less the same, converging on the common pool of ethny-specific genetic structures.  So, while in the first generation, your offspring and that of your brothers may be distinct with respect to genetic structure, that difference would be attenuated over time and, as long as endogamous mating is maintained, your posterity and theirs would reflect similar genetic structures.  But there are problems here.  First, a rigorous analysis is required; perhaps some differences would continue over at least several generations; even if these differences are small, they nevertheless would need to be accounted for.  Second, if it is true that familial genetic strictures would tend, over time, to converge on more generalized ethny-specific structures, then why bother favoring two brothers over two random co-ethnics?  The brothers would share more of your genes, yes, and be more similar as far as genetic structure, but if one invokes “long term intergenerational effects” with respect to questioning the need to account for structure in modifying Haldane’s argument, then one can use the same “intergenerational effect” to directly question Haldane’s original premise.  The answer I believe is that one must do the best they can at a given time in maximizing their genetic payoff, and hope that subsequent generations do the same. In the absence of the required analysis, one can simply argue that looking to the next generation, differences in genetic structure are important and, hence, two brothers are not quite the genetic equivalence of yourself.  Your structure is different from theirs and the genetic payoff of your reproduction is greater for your than both of theirs combined.  So, maybe you need to hold out and sacrifice for three (or more) brothers instead, including for the other reason outlined above. Note that these fine points deal with very close genetic similarity.  When we are talking about racially alien peoples, the genetic distance becomes even more amplified with genetic structure, and in the absence of panmixia, ethny-specific patterns of genetic structure are broadly stable over evolutionary time (we can see that the Iceman is genetically more similar to Europeans than to, say, Asians  of Africans, as one example).

In the absence of the sort of careful quantitative analysis that population geneticists won't do, from a qualitative standpoint, it would be prudent to require more of a genetic payoff before engaging in Haldane-style altruistic self-sacrifice.  On the other hand, when considering a choice in investing between two genetic entities, picking the group genetically closer to you is even more important when considering genetic structure.  So, when the choice is between self vs. family or family vs. ethny, genetic structure will require a larger genetic payoff before agreeing to sacrifice the interests of the former for the latter. However, when considering a relative choice between ethny one vs. ethny two, genetic structure means that choosing the more similar-to-you ethny is even more important than with "bean-bag" genetics.  

The overall Salterian imperative remains the same as before, once these adjustments are made.

Yet Even More DifferInt

More DifferInt model results.

Note that genepool is exactly the same between both populations, but rearranging genotype combinations gives some differentiation at single and multiple locus measurements even when including elementary genic differences, and there is complete differentiation at the level of multiple locus genotypes neglecting elementary genic differences, even though the genepools are identical and there is not a very large number of genotype rearrangements between the populations. This shows how rapidly complete differentiation is achieved when considering discrete genotype combinations.

(A = 1, T = 2, C = 3, G = 4, first number = number of individuals per genotype)

 #Population1

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  4 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  4 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  3 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  3 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

#Population2

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  3 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  3 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1 2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  4 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  4 4

Genepool: 0.0000

Single locus including elementary genic differences: 0.0167

Single locus neglecting elementary genic differences: 0.0333

Multiple locus including elementary genic differences: 0.0410

Multiple locus neglecting genic differences: 1.0000

Yet More DifferInt

More on genetic integration.

Some interesting quotes from this paper; emphasis added:

The elementary genic difference does not distinguish homologous from non-homologous genes. Hence, the homologous and non-homologous gene arrangements within the objects affect the elementary genic differences between them only through their sum. For example, in the case of diploid individuals scored at two gene loci A and B, say, the genotypes A1A1/B1B2 and A1A2/B1B3 represent three (A1, B1, B2) and four (A1, A2, B1, B3), respectively, of the total of five gene-types. A1 is represented by two copies in the first genotype and by one copy in the second, and the remaining four gene-types are represented by at most one copy in each of the two genotypes. The sum of copy number differences between the two genotypes thus equals four. After division by twice the number of individual genes in a genotype (i.e. 2·4), this yields 0.5 as the elementary genic difference. The same result is obtained for the two genotypes A1A2/B1B2 and A1A2/B3B3, even though all genic differences are now due to the alleles at a single locus (B). 

Proceeding from lower to higher levels of integration, one expects an increase in differentiation among populations simply because of the larger varietal potential inherent in more complex structures. Since differentiation is based on distances, the distance between two populations should therefore also increase, or at least not decrease, with integration level. 

…it appears that differentiation among populations with respect to their forms of gene association may be a normal occurrence. This insight questions the common practice of restricting the measurement of population differentiation to the allelic level (e.g. FST), thereby ignoring the considerable effects of gene association on population differentiation.

One major finding of the paper is that model data routinely give no increase in differentiation (measured including elementary genic differences) with increasing genetic integration, but real data does show increases.  One wonders if large scale human SNP data would demonstrate such differences, as opposed to the limited SNP data or model systems I have used, which demonstrate increased differentiation only when elementary genic differences are neglected.  On the other hand, as I’ve previously written, neglecting elementary genic differences is, I believe, more compatible with my idea of genetic structure.

That said, one can, if they choose allele structure carefully, produce models that do the exact opposite, have equality at the lower levels of genetic integration, but differentiation at the highest level.

Here is an interesting population model I devised and tested with DifferInt; the differences between the two populations are highlighted.  Note that total numbers of each allele are the same, and the total numbers of single locus genotypes are the same as well.  Thus, genepool differentiation is zero (0.000), as is single locus genotype differentiation, also zero (0.000).  The arrangement of the first and ninth single locus genotypes, together, were changed in six of ten individuals between the two populations, thus producing differentiation specifically at the level of multilocus genotypes. 

(A = 1, T = 2, C= 3, G = 4; first number = number of individuals) 

MLG with EGD: 0.0246

MLG w/o EGD: 0.6000 (6/10 individuals per population altered)

#Population1

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

#Population2

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  3 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 2  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1 2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

1  1 1  2 2  2 3  3 3  1 1  1 4 1 1  2 2  2 3  3 3  1 1  1 4

More Genetic Structure and DifferInt Analysis

An important topic.

I have been looking a bit more at the DifferInt program (currently unable to find anything better), testing some model genotypes to better understand the relationship between different levels of integration with respect to the amount of differentiation.  One finding which is clear that it is when genetic differentiation – at the lowest genepool level - between groups is shallow is when the program is scalable at the level of the highest level of integration.

A test model was devised with two populations of eleven individuals each.  Six loci were considered.  Initially, the two populations were constructed to be genetically identical. Four individuals of the second population had alleles at one lock rearranged so that four heterozygotes were made into four homozygotes (two of each type), without changing the total number of each allele type for that locus in that population.  After this change, the genepool differentiation was 0.0303, but the multilocus genotype neglecting elementary genic differences (MGNEGD) was 0.3636 – a twelve-fold increase in differentiation.  In this simple model of shallow genetic difference, a discrete representation of genetic structure (MGNEGD) is seen to exhibit sharply increased (and quantitatively scalable) differentiation with even a small change in allele structuring in genetically similar (model) populations.

However, when differentiation at the genepool level is already fairly high, then MGNEGD rises to complete differentiation quickly, and the ability to evaluate genetic structure becomes non-scalable using this program.  It could be that the SNP database I utilized for my initial human study was enriched in SNPs that sharply differentiate between ethnies and so all levels of differentiation were high in the analysis; perhaps completely random SNPs would be better? On the other hand, we are most concerned about the distinctive genome (with respect to EGI).  

In a more realistic model of human genetic differentiation, two populations were set up, each consisting of ten individuals, each assayed over 100 loci.  90 of these loci were absolutely identical between the two populations and 10 loci differed between the populations with respect to the frequencies of alleles at the loci.  In some cases, it was 100%  of one allele pair compared to 100% of another; in other cases it was more subtle - for example one population having 20% AA, 60% AT, and 20% TT while the other population was 20% AA, 50% AT, and 30% TT for the same locus.  The genepool differentiation between the two populations was 0.0370; the MGNEGD was 1.000 - complete differentiation.  This again shows that with enough loci studied and differentiated populations, analysis of discrete sets of multilocus genotypes (see my definition of genetic structure below) will reach complete differentiation.  The implications for genetic interests should be obvious.

It might be a good idea to review my idea of genetic structure again here.

Genetic structure as per my definition can be viewed as a form of linkage disequilibrium of alleles over all the loci in the genome, or this distinctive genome, of at least whatever number of loci that were assayed.  Each specific permutation of multilocus genotypes is a discrete entity, so that one would expect, of course, district genetic structures between any set of individuals who are not identical twins; there would be differences in genetic structure within families, never mind within ethnies.

However – and this is the key point that separates my idea from the run-of-the mill evaluations of genetic structure - I envision genetic structure to be defined by specific ranges of multilocus genotypes.  Therefore, while there is going to be, naturally, individual variation of discrete multilocus genotypes within families, there will be a family-specific range of multilocus genotypes, a range within which all the individual genotypes, of that family will fall within.  Likewise, there will be ethny-specific ranges of multilocus genotypes, so that members of an ethny will exhibit genotypes that – while they differ on an individual level – will fall within a range, a set, of genotypes characteristic of that ethny.  

It then follows, that while multilocus genotypes will be differentiated from each other, the extent of that differentiation will differ.  Different families will exhibit different ranges, or sets, of possible multilocus genotypes, but families belonging to the same ethny will exhibit ranges that are more similar to each other than that of families of different ethnies (the same goes for individuals of course, across families or across ethnies).  Ethnies belonging to the same continental population group (i.e., intra-racial) will exhibit more similar ranges of possibilities of multilocus genotypes than that of inter-racial comparisons.  One could think of it also as frequency distributions of multilocus genotypes, of all the alleles possibilities at all the relevant loci considered together as a discrete entity, and one can compare how similar the frequency distributions are, with more overlap from those more similar.  

One would also expect a solid correlation, or association, between the differentiation as measured by an allele-by-allele genepool/beanbag approach, single locus genotypes, and multilocus genotypes. The relative extent of differences should correlate in at least a qualitative sense between these levels of “genetic integration.”  Hence, as previously noted at this blog, “complete differentiation” at the multilocus genotype level should differ in extent dependent upon how similar or different the genotypes are from each other.  One should in theory be able to quantitate this in a continuous fashion, rather than just having a binary yes/no undifferentiated/completely differentiated choice.

This is obviously an important topic.  If we are to make decisions based on genetic interests, don’t we need to have a better understanding about what those interests actually are, quantitatively speaking?

It’s true that we know enough right now to justify taking action in defense of genetic interests; even at the lowest levels of genetic integration, and even with estimates of child equivalents based on Fst, we already know that mass migration of alien peoples is genocide.

So, yes, I’m sympathetic to the argument that in general, qualitatively speaking, it is more important to actualize a defense of the interests we already know about than to fine-tune our understanding of these interests. But why not both?  Nothing stops us from both organizing on a political and metapolitical level while at the same time continuing to refine our understanding of this topic.  While most of my work now concerns the political and metapolitical implications of defending EGI and of actualizing a High Culture, surely there is also a place for a better understanding of EGI and for a better understanding of Spenglerian cycles and how to control them foe civilizational benefit.

Genetic Detection of Immigrants

Multilocus genotypes.

Detecting immigrants from the analysis of multilocus genotypes: paper here.  An old paper; of course, methodology has gone past this since; nevertheless, it deserves to be noted, for the idea that looking at multilocus genotypes allows for distinguishing genetic types even when "bean bag genetics" differentiation is low.  The basic premise; emphasis added:

Immigration is an important force shaping the social structure, evolution, and genetics of populations. A statistical method is presented that uses multilocus genotypes to identify individuals who are immigrants, or have recent immigrant ancestry. The method is appropriate for use with allozymes, microsatellites, or restriction fragment length polymorphisms (RFLPs) and assumes linkage equilibrium among loci. Potential applications include studies of dispersal among natural populations of animals and plants, human evolutionary studies, and typing zoo animals of unknown origin (for use in captive breeding programs). The method is illustrated by analyzing RFLP genotypes in samples of humans from Australian, Japanese, New Guinean, and Senegalese populations. The test has power to detect immigrant ancestors, for these data, up to two generations in the past even though the overall differentiation of allele frequencies among populations is low.

Classical theory in population genetics has focused on the long term effects of immigration on allele frequency distributions in semi-isolated populations, concentrating on the stationary distribution resulting from a balance between forces of immigration, genetic drift, and mutation (1–4). Less theory exists addressing the effect of recent immigration among populations with low levels of genetic differentiation. A theory describing the effects of immigration on the genetic composition of individuals in populations that are not at genetic equilibrium is needed to interpret much of the data being generated using current genetic techniques. 

In this paper we consider the multilocus genotypes that result when individuals are immigrants, or have recent immigrant ancestry. We propose a test that allows recent immigrants to be identified on the basis of their multilocus genotypes; the test has considerable power for detecting immigrant individuals even when the overall level of genetic differentiation among populations is low. Molecular genetic techniques that allow multilocus genotypes to be described from single individuals are relatively new, and much of the information contained in these types of data is not fully exploited by estimators of long term gene flow that are currently available (5–7). We provide an example of an application of the method to restriction fragment length polymorphism (RFLP) genotypes from human populations; the method may also be applied to analyze multilocus allozyme and microsatellite data.

Also:

 At least three potentially misleading results may arise when applying the method considered here. First, the failure to reject the hypothesis that an individual was an immigrant, or descended from immigrants, may simply reflect the fact that the appropriate populations for comparison were not included in the analysis. Second, an individual might incorrectly appear to have originated in a particular population other than the one from which it was sampled. This might be due to similarities in allele frequencies, due to long-term gene flow, between that population and a third population from which the individual actually originated, but which was not included in the sample of populations. Third, the fact that many pairwise comparisons between populations are performed for each of a large number of individuals means that some individuals will appear to be immigrants purely by chance.

See this as well.  And also this.

In the late 1990s and early 2000s, there was some work going on in population genetics concerning multilocus genotypes.  A lot of good could have come from that if it was continued.  By an interesting coincidence, work on this subject essentially ended around the same time Der Movement and the HBDers went online talking about, and dissecting, population genetics studies.  It could be a coincidence, but given how most population geneticists are hysterical SJWs, maybe some of them decided not to investigate areas of their field that would focus attention on the great degree of actual ethnoracial differentiation that exists when genetic structure is taken into account.