Category: genetic variation

An Empirical Racial Soul?

A brief materialist look at “spiritual race” mechanisms.

Readers of this blog are probably aware that I – a scientific materialist and empiricist – am critical of “spiritual race” theories, including ideas about a “racial soul” or “race soul,”  whether these are derived from Spengler, Yockey, Evola, or German Nazism.

However, is there perhaps an area of overlap between biological and spiritual race theory, one in which ideas of a “racial soul” and “spiritual race” – an innate sense of self, instinctive behaviors and preferences, and metaphysical beliefs and aspirations connected to particular ethnies – have some sort of discoverable, knowable, physical basis, a materialist foundation?  In other words, spiritual race exists but is not something independent of matter and of the physical body but is a derivation of it; the race soul being an emergent property of biological racial characteristics, influenced by culture and a people’s history, their “genetic memory” as a ethnocultural-historical entity.

One could speculate that characteristics of a “racial soul” are influenced by:

1. Genetics; complex epistasis of many gene variants and their expression that influence behavior in a manner beyond the current level of understanding of definitive “genes that affect behavior.”

2. Epigenetic influences that are stable over time because they are constantly reinforced by cultural/historical/environmental factors, some of which are themselves influenced by epigenetics (self-reinforcing) or underlying genetic differences (gene-culture effects and canalisation).  

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.

3. Learned behaviors, passed down through the generations, which appear instinctive and unlearned because they are long-term, subtle and complex, and hence invisible to casual and immediate observation.

4. The combination of 1,2, and 3 so as to produce reproducible ethnic and racial traits that are seemingly unconnected to strict biological race, and seemingly so because the level of analysis is superficial and only looking at direct and immediate relationships between “one gene and one phenotype.”

Please note that if complex “cross-talk” exists between culture/environment on the one hand, and genetics/epigenetics on the other, manifested as a “racial soul” – or “spiritual race” – then by altering a group’s culture and environment, one can change the underlying physical basis of their racial soul.  Is one reason for the degeneration of Whites in recent history – their complete spiritual and moral collapse – due to the poisoning of their culture and the decay of their environment due to Leftist/Jewish influences?

Also note that given variability within a race as regards genes and epigenetics, and different life experiences of individuals, outliers of the racial soul can exist (as noted, e.g., by Yockey and Evola) – a member of one “biological race” belongs to a different “spiritual race” – mechanistically explained by unusual combinations of influences 1-4 listed above.  But for an entire group, and most of its members, the racial soul should be consistent (and also, unfortunately, consistently susceptible to degeneration).

At this point, it is imperative to further consider “cross-talk” between genes and culture, and between epigenetic influences, genes, and culture, and the process of “canalisation.”

Canalisation is a measure of the ability of a population to produce the same phenotype regardless of variability of its environment or genotype. It is a form of evolutionary robustness. The term was coined in 1942 by C. H. Waddington to capture the fact that “developmental reactions, as they occur in organisms submitted to natural selection…are adjusted so as to bring about one definite end-result regardless of minor variations in conditions during the course of the reaction”. He used this word rather than robustness to take into account that biological systems are not robust in quite the same way as, for example, engineered systems. 

Biological robustness or canalisation comes about when developmental pathways are shaped by evolution. Waddington introduced the concept of the epigenetic landscape, in which the state of an organism rolls “downhill” during development. In this metaphor, a canalised trait is illustrated as a valley (which he called a creode) enclosed by high ridges, safely guiding the phenotype to its “fate”. Waddington claimed that canals form in the epigenetic landscape during evolution, and that this heuristic is useful for understanding the unique qualities of biological robustness.

Thus, it is part of the racial soul to reproduce the same phenotype regardless of variation in the environment, or even regardless of fluctuating variation (e.g., from genetic drift, bottlenecks, etc.) in the genotype – as long as certain core components of the genotype remain intact.

Also consider the related hypothesis of “evolutionary capacitance.”

Evolutionary capacitance is the storage and release of variation, just as electric capacitors store and release charge. Living systems are robust to mutations. This means that living systems accumulate genetic variation without the variation having a phenotypic effect. But when the system is disturbed (perhaps by stress), robustness breaks down, and the variation has phenotypic effects and is subject to the full force of natural selection. An evolutionary capacitor is a molecular switch mechanism that can “toggle” genetic variation between hidden and revealed states. If some subset of newly revealed variation is adaptive, it becomes fixed by genetic assimilation. After that, the rest of variation, most of which is presumably deleterious, can be switched off, leaving the population with a newly evolved advantageous trait, but no long-term handicap. For evolutionary capacitance to increase evolvability in this way, the switching rate should not be faster than the timescale of genetic assimilation.

This mechanism would allow for rapid adaptation to new environmental conditions. Switching rates may be a function of stress, making genetic variation more likely to affect the phenotype at times when it is most likely to be useful for adaptation.

Different ethnies contain different types of, and levels, of such genetic variation; hence, human groups differ, qualitatively and quantitatively, in their evolutionary capacitance.  What this means in terms of a “racial soul” is that different groups may not reflect a type of phenotypic difference in one environment, but once exposed to a different, stressful environment, robustness breaks down and the inherent genetic variation is expressed in phenotypes previously masked.  This expression of masked phenotypes is one manifestation of the “racial soul.”

Note that canalization and evolutionary capacitance reflect the concept of a racial soul in opposite manners.  The former describes the robustness, the consistent replication, of racial behavior and racial expression in various environments (with perturbations within limits) – thus, different ethnies will consistently reproduce aspects of their racial souls even when transplanted to new living spaces, such as groups migrating to the same common territory (e.g., America).  The latter concept describes situations in which differential expression of a racial soul is masked, hidden, because canalization stabilizes phenotypic expression within a particular environment, but this expression of the racial soul is unleashed upon transition to a more radically different environment.  Thus, different groups, which appear similar in behavior on the surface, will reveal radically different behaviors – seemingly instinctive behaviors – for example in times of war, upheaval, or even radical changes in cultural paradigms.  

Both poles of racial expression – the robustness of canalisation in which the revealed states are stable within a certain degree of environmental variation and the unleashing of hidden states of racial expression built up through evolutionary capacitance – should have materialist, physical explanations.  Canalisation is due to gene-culture co-evolution (with perhaps epigenetics playing a role), while evolutionary capacitance is due to inherent genetic (and possibly epigenetic) variation of ethnies that creates the potential for behaviors that, hidden at one time, become revealed and expressed at another time.

Both of these poles of expression – the uncanny consistency of group expression and the hidden abilities of groups that become revealed in times of stress – can be considered aspects of race typically labeled as “spiritual race” and the “racial soul.”

On related notes, see “genetic memory” (mentioned above) – also discussed here – as well as Jung’s “collective unconscious.”  If we are to seriously consider these ideas from the standpoint of materialist biological science, then the same mechanisms discussed above likely apply.

With sufficient understanding and technical advances, it may be possible at some point in the future to evaluate these ideas, and determine whether there is an underlying material basis – actual physical mechanisms – for these postulated phenomena, and, more fundamentally, determine the validity of the actual existence of these phenomena for the human condition.  In other words, does a “racial soul” really exist and, if so, what is its physical, mechanistic basis?

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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 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.

More Problems With Fst

More Fst follies.

Commonly used measures such as FST and its derivatives based on gene identity probabilities do not reliably reflect difference, as they can be maximal when almost all populations are identical and very small when populations are completely distinct.

I’ve been saying this for years, citing other papers, noting the stupidity of people like J Richards of Majority Rights, who was breathlessly pontificating about minute differences in Fst values – a metric that cannot reliably determine genetic differentiation, since it is dependent upon the genetic variation within groups; it essentially is more about the apportioning of genetic variation within and between groups.

But all of this won’t stop Der Movement “activists” from using discredited metrics when it serves their purposes.