Category: James Bowery

Social Epistasis

This ranks among the most important sets of work I have reviewed.

I do not want to be churlish, so I’ll admit that I was alerted about this paper through the website Chateau Heartiste (ironically, since the nihilistic hedonism of “game” contributes to the problems outlined in the paper).

The paper is more of a HBD-style analysis, not my usual “cup of tea,” but is nevertheless useful since it an effective counter to atomized individualism of all types – the rightist libertarian form, the anti-Salterian HBD form that asserts that (for Whites) only individual and family interests matter and that the ethny is irrelevant, the leftist form in which extreme individualism is promoted with respect to ethny but hypocritically collectivism is promoted with respect to humanity as a whole.

I have read the paper, which can be seen to have a rightist perspective, and even cites the work of Kevin MacDonald.  Indeed, with sections on “pathological altruism” and “free-riding” it almost reads as something one would find at The Occidental Observer or EGI Notes, or perhaps something written by Frank Salter.  What are its major points?

Mutational load increases from generation to generation as a consequence of normal biological processes, and this is exacerbated by the tendency, in Western populations, for people to become parents later in age, since gamete mutations increase with age. Note that when these mutations exert a phenotypic effect, in the great majority of cases the effects will be negative. In order to avoid “mutational meltdown” as a consequence of accumulation of deleterious alleles, purifying selection is required, and in theory such selection would require that the vast majority of the population not reproduce (with the more genetically healthy remainder making up the population shortfall via increased reproduction).  The authors suggest that a numerically more realistic solution would be a form of “cryptic” purifying selection, in which those who have a greater mutational load are less likely to reproduce and/or have less children if they do reproduce, than those with fewer mutations (not necessarily and “all or nothing” situation but more of relatively suppressed fitness consequent to a heavier mutational load).  The authors cite evidence that increasing parental age – resulting in increased numbers of mutations carried by sperm – result in offspring more likely to have behavioral defects or decreased physical attractiveness.  Given that the authors suggest that sexual selection in mate choice can be a honest assessment of genetic quality (one can quibble with this in modern society in which women sometimes prefer low-IQ colored “alpha male” brutes, but this quibble may actually be consistent with the authors’ belief that selection has been compromised in modern society), then over time higher mutational load would be selected out.  

Given that many genes – including mutated alleles – have pleiotropic effects (influencing multiple traits at the same time), this could be quite efficient, since selection exerted on any of the various traits would affect selection on those alleles causing a wide variety of negative phenotypes and selecting against all those phenotypes simultaneously. Conversely, I might add, this also helps by having the mutated alleles being targeted by selection at any one of several traits, increasing the probability of the allele in question being selected against, targeted as it is by convergent selective pressures generated by the interaction of the phenotypes with the environment.

In this scenario, only a minority of the population would have to go childless for this to work, and in the past, Western populations demonstrated a reproductive pattern (who mates, what children survive to adulthood), consistent with selection against excessive mutational load. However, the authors assert that this process has become short-circuited in modern society, in which most people mate and reproduce, and most children survive to adulthood, and that environmental, social, and cultural factors can alleviate some of the negative effects of mutational load (e.g., medications, medical care, cosmetics, etc.).  Thus, modern society does not effectively select against mutational load, but merely reduces the cost of that load on the affected individual.  Thus, a high-loaded person is not selected out of the population but is instead “propped up” by society’s infrastructure, reproducing, and adding to the load in the next generation.  This is not unexpected.  After all, the authors cite work with fruit flies that show that those strains with higher mutational load can suffer up to a 10-fold decrease in fitness in competitive environments compared to a lack of competition that selects against mutation. In modern society, in which “all life is valued,” which do you think holds?

On a purely anecdotal personal note, I’m amazed how frequently I see individuals derived from “Western populations” – usually younger people – who seem to reflect a high mutational load. I often observe individuals of ostensibly normal or even high intelligence who have the physical appearance of Down syndrome and who at the same time display semi-autistic behavior.  Also, the whole SJW “snowflake” phenomenon, particularly on college campuses, perhaps reflects behavioral aberrations derived from mutational loading. Extrapolating this genetic deterioration into the future leads one straight to idiocracy.  Even more extreme, a complete biological collapse, leading to human extinction, is possible.

What costs to society accrue based on this?  The authors cite suggestive evidence for declining quality of Western populations, including increases in the prevalence of autism and ADHD, increased skeletal asymmetry and left-handedness, the rise of obesity, and various medical abnormalities. Intriguingly, they also suggest that the “demographic transition” – the below replacement fertility of Western populations – may be not only due to cultural factors and “rational choice” mechanisms, but also due to changes in the “fitness characteristics of the group-level extended phenotype of modern populations” (emphasis in the original, and a phrase not out of place at this blog or the work of similarly-minded individuals) so that deleterious mutations accumulating from “ecological mildness” cause  =(directly or indirectly) “fertility transition” resulting in a “very rapid fitness collapse in Western populations…”  To put in bluntly: we created an advanced “ecologically mild” society that relaxed selection against the botched and unfit, resulting an aberrant extended phenotype at the group level, causing group extinction and race replacement.  

Since the authors bring up group selection, they then briefly discuss the “selfish gene” (Dawkins-HBDer view) vs. the “group selection” view, citing the issue of “free-riding” oft-discussed at this blog and also in the work of Frank Salter and Kevin MacDonald.  The authors reasonably support the idea of “multilevel selection” – in that in some cases selection works at the individual level (e.g.., in peacetime) and at other times at the group level (e.g., in warfare).  In today’s globalist world with a Clash of Civilizations, mass migration, and race replacement, guess which level is more relevant? Even though group selection is not required for EGI, the fact is that the world environment is such that group selection must be the predominant fitness mechanism extant today.

Next, the topic of social epistasis.  Epistasis typically describes gene-gene interactions within a single organism, while social epistasis describes such interactions taking place between organisms.  After a discussion of eusocial insects, the authors speculate on the human situation, and the possibility that human societies require particular forms of social epistasis for optimal function and maximal fitness. In healthy societies, high-status individuals generate and promote free-rider controls – e.g., religions and/or ideological systems that promote behavior that benefits the group and repress behaviors that selfishly benefit only the individual.  Behavior so cited include “ethnocentrism, martyrdom, and displays of commitment.”  Also important is so-called “effortful control” – the ability of humans to control their behavior and impulses so as to act to benefit the group.  On the other hand, mutations can break down the affinity of high-status individuals for the group – which I note we see today in the West with the complete treason of the elites against their own ethnies – thus “causing dysregulation of the group’s reproductive ecology” – hence the demographic trends we see today.  And although I myself am no fan of religion, I note the authors cite religion as a positive controlling force and postmodernist “individualistic, secular, and antihierarchical values” as negative. 

Of great importance is the emphasis the authors place on control of free-riding as a component of a healthy society exhibiting optimal function and fitness, and how breakdown of free-riding control, perhaps through mutational loading, reduces societal function and fitness.  Consider the importance given control of free–riding in the work of Frank Salter and Kevin MacDonald, and my support of their work, and draw your own conclusions as to the great validity of that work compared to its deluded or mendacious critics.

I also note that the authors mention “spiteful mutations” – having effects that harm others while not benefiting the individual possessing the mutation or even also harming that individual – as those which may act to remove constraints on free-riding.  Indeed, it is possible that the person with the free riding-enabling mutation is not the actual free-rider, and in fact the mutant individual may be harmed by the free-rider.  One can speculate here about White mutants that harbor spiteful mutations that enable Jewish/Colored/atomized White free-riding, thus harming all Whites, including the mutant Whites themselves.

Next on the agenda is a topic near and dear to our hearts: pathological altruism.  The authors state that “cultural disturbance” (i.e., the modern “West”) can promote “maladaptive personality traits” leading to pathological altruism and/or the removal of constraints on free-riding. Cited as examples are self-righteousness (cue the SJWs) and narcissism (indeed, the Dark Triad is invoked here as a problem, ironic given the forum from which this paper came to my attention).  One behavior in particular cited by the authors is the “clever silly phenomenon” of “virtue signaling” utilizing “counterfactual beliefs,” including the moralistic fallacy of “the conflation of moral equality among individuals, sexes, and populations with biological equality” (and the related moralistic fallacy of race denial).  

Indeed, the authors speculate that there may be an increased number of individuals in modern Western societies prone to spreading such silliness, and that “Machiavellians and narcissists” seem uniquely advantaged to achieve elite status in today’s world, thus further promoting memetic flotsam and jetsam. Thus we observe “elite egoists” encouraging “selfish behaviors” previously restrained by belief systems (e.g., religion).  Indeed, a feedback loop may exist where mutation directly or indirectly increases egoism; the egoists rise to influence, and then use their power to alter the sociocultural environment to “foster norms that are friendly to egoism and thus magnify opportunities for other egoists to obtain cultural capital.”  Sound familiar? (And we can cite an ethnic dimension to his – cue the work of Kevin MacDonald).  Included in this cultural capital are anti-natalistic memes (also found in the “movement”) and the related “morality of self-fulfillment.”  We can of course more directly cite the pathological altruism of cucked xenophilia, leading to mass migration and race replacement  Related to all of this is a loss of “effortful control,” so people lack the ability to retrain their destructive behavior.  

The authors include a figure at this point; the figure legend includes:

Flowchart illustrating the pathways through which accumulating deleterious mutations can suppress fitness. Mutations can reduce (as the minus sign indicates) intrinsic/genetic fitness directly, in addition to promoting (as the plus sign indicates) behavioral change. Behavioral change can further directly suppress individual-level fitness while simultaneously promoting the degradation of group-level regulatory processes (e.g., free-rider controls), via social epistasis. This degradation feeds back into fitness, both directly (via its direct effects on group-level fitness) and indirectly (via facilitation of further behavioral change) imposing additional costs on fitness. Behavioral change, resulting either directly from mutations or the breakdown of group-level regulatory processes, can also rebound on intrinsic fitness via its promotion of mutation accumulation.

This is followed by mathematical modeling demonstrating how the sizes of different populations can be altered as a result of carrying deleterious mutations.

Finally, in the Discussion, the authors quote another researcher who stated that “the brain is a particularly large mutational target” so that behavioral changes due to mutation are to be expected. Social epistasis is a vulnerable target for spiteful mutations, leading to significant depression of society fitness, as demonstrated by Western demographic decline, particularly among high-status, high-IQ individuals (remember that spiteful mutations can harm the fitness of those that carry them and not only harm others).  Modern society and its advancements have reduced selective pressure, allowing the spread of deleterious mutations and the consequent release of constraints on free-riding, reducing the optimal function of the group and greatly reducing group fitness.

The authors relate their thesis to Calhoun’s mouse utopia experiments, and the parallels between the collapse of the mouse utopia and the collapse of the modern “West” are striking.  For example, the “decline phase” of the mouse utopia was characterized by the emergence of animals called the “beautiful ones” that exhibited “apparently bizarre behaviors” including “obsessive grooming, hyposociality, and asexuality.”  Let’s consider the human equivalents: metrosexuals, atomized Whites and the even more extreme anti-social autistic spectrum, and the rise of transgenderism and celibate beta males.  

The authors quote Calhoun concerning the spiritual and then physical death of the mouse utopia:

Autistic-like creatures, capable only of the most simple behaviors compatible with physiological survival, emerge out of this process. Their spirit has died (“the first death”). They are no longer capable of executing the more complex behaviors compatible with species survival. The species in such settings dies.

Behold the Death of the West.

The authors conclude that the issue of mutational load is a serious problem worthy of further study.  Indeed, it is, but is not the only problem that one can derive from a close reading of the paper.  

Related to the above is this paper, summarized here (*), the author summary of which is as follows (emphasis added, and you can read both papers yourself, as I am going to only very briefly discuss there here):

Daily interactions between individuals can influence their health both in positive and negative ways. Often the mechanisms mediating social effects are unknown, so current approaches to study social effects are limited to a few phenotypes for which the mediating mechanisms are known a priori or suspected. Here we propose to leverage the fact that most traits are genetically controlled to investigate the influence of the social environment. To do so, we study associations between genotypes of one individual and phenotype of another individual (social genetic effects, SGE, also called indirect genetic effects). Importantly, SGE can be studied even when the traits that mediate the influence of the social environment are not known. For the first time we quantified the contribution of SGE to more than 100 organismal phenotypes and genome-wide gene expression measured in laboratory mice. We find that genetic variation in cage mates (i.e. SGE) explains up to 29% of the variation in anxiety, wound healing, immune function, and body weight. Hence our study uncovers an unexpectedly large influence of the social environment. Additionally, we show that ignoring SGE can severely bias estimates of direct genetic effects (effects of an individual’s genotypes on its own phenotype), which has important implications for the study of the genetic basis of complex traits.

Thus, the genetic makeup of those in your environment can affect your phenotype – that is the expression of your own genes in response to the environment, said environment also consisting of the genetic makeup of those around you.  To say this finding is remarkable would be a gross understatement.  And why not extend this paradigm to the group level? – the genetic makeup of one group in a territory can affect the phenotypic expression of another group’s genepool.  Perhaps James Bowery and I (with Bowery being the one who should be given credit for introducing the paradigm) were correct in using extended phenotypes to explain various human behaviors, including the White extended phenotypes of Jews and Coloreds.  The implications should be obvious – one group’s genetic structure can be a weapon through which a second group’s fitness is depressed by manipulation of that second group’s phenotype, e.g., by promoting maladaptive behavior on the part of the second group.  Examples can include Jewish and Asian manipulation of the behavior of Whites.

This synergizes with the social epistasis paper, since mutational load – resulting in, e.g., pathological altruism – can make one population vulnerable to the social genetic effects of another population.

*Key points of the summary:


These experiments with mice highlight opportunities and challenges for social genetic research in humans. One opportunity is to investigate social genotypes as environmental measures. There is already human research investigating social phenotypic effects, e.g., the social “contagion” of obesity (“Are your friends making you fat?”)…In addition to direct effects of the social environment/genome, synergies between social and personal genetics are possible. Specifically, social genotyping could be used to study interactions between a person’s genes and the genes of socially proximate individuals…A primary issue is the extent to which social genotypes are independently determined. Individuals who share traits may be more likely to sort into social units together, a phenomenon called homophily…Thus, while SGEs may shape an individual’s phenotype or modify the phenotypic effects of that individual’s genes, reverse causation is also possible; i.e., an individual’s phenotype and/or genotype may shape the genetic composition of their social environment…

That is also all remarkable and again something one would expect coming from Kevin MacDonald, Frank Salter, or myself.  Homophily – the foundation of the ethnostate?  The reverse causation reminds one of this article, written by a very sagacious individual.

Thus, the summary underscores the points about social genetic effects, and also underscores the basic meaning behind the social epistasis paper – that is, no man (or woman) is an island.  We – and by “we” I mean on both an individual and group level – affect each other on the most basic levels of genotype and phenotype.  Atomized individualism is exposed as a fraud, a mockery, a pipe-dream, a fantasy, with the reality being one of deep connections between the genotypes and phenotypes of various individuals and groups, modified by the mutational landscape, driven by social epistasis, and resulting in shifts in the relative fitness of individuals and groups.  Further, the interactions between genes and the “social environment” are bidirectional; hence not only does the environment shape the demographic composition of the population within it, but that population shapes the environment, making that environment more or less congenial for certain types of individuals and groups compared to others. In the end, all the “who cares” arguments with respect to race and EGI are exposed as either deception or self-deception. In a social species such as humans, “rugged individualism” (OK as far as it goes, within limits, as a concept for personal self-improvement) cannot be inflated into social policy, as it goes against scientific fact and objective reality.  That reality may be harsh to those who wish to hold onto cherished illusions – or to those who have a vested interested in peddling those illusions to others – but harsh or not, that reality is what we have to deal with. Failure to deal with reality will result in replacement by those unencumbered by illusion and less susceptible to being fooled by the deceptions of others.

The sort of policy initiatives to combat the problems outlined in these papers – initiatives that would actually work – would tend to fall on the, let us say, right of the political spectrum.  A complete biocentric reordering of society is required.  Following current trends will not only lead to cultural and social collapse, but genetic-biological collapse as well.  The stakes couldn’t be higher.

Finally, these papers support the ideas and the work of the following individuals: Frank Salter, Kevin MacDonald, James Bowery, and Ted Sallis. On the other hand, the anti-Salterian HBDers are once again soundly refuted, although they will of course not have the good grace to admit error.  And while I do not want to engage in Frankfurt School-style pathologization of the other side, these works raise the question whether critics of EGI are suffering from a heavy mutational load and/or are trying to influence others so afflicted.

It are the aforementioned four individuals who are on the side of human progress and who are moving to the light, while those others peddle a recipe for death, decay, destruction, and darkness.

Which side are you on?

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Remember the Rhizome

The importance of preserving the rhizome.

Read this and focus on the difference between the organized slime mold model of “fascist” activism, and the rhizome model of decentralized groupuscules.  Keep in mind that the EGI Notes-Western Destiny axis is an example of a groupuscule (population of one). The ultimate fascist slime mold?  National Socialist Germany, I suppose.

What’s the immediate future of groupuscles – the decentralized rhizome structure – in today’s context?  Are we transitioning to a more slime mold like structure, with the rise of the Alt Right and Trump? Are groupuscules affecting mainstream politics via the Alt Right to Alt Light (and Alt Wrong) to Civic Nationalist Trump continuum?

I argue that we need both slime mold and rhizome. Especially today, when there is a great power disparity between the System and Der Movement, it is prudent for Der Movement not to put “all its eggs on one basket” – or to have just one big egg, which can end up like Humpty Dumpty.  It is prudent to allow for a variety of memes to be generated and tested, here I call for Bowery’s “sortocracy” within Der Movement itself.  Let’s test various ideas instead of smothering them within the overarching “movement” dogma that has failed over and over again for decades.  The importance of having diverse ideologies in Der Movement is outlined in this excerpt from my essay:

The decentralized aspect of the current far right allows for the development of diverse, interesting, and extremely varied permutations of memes and ideology—manifestations that would not be possible in the context of a highly organized, top-down hierarchical structure imposing a common worldview. While most “movement” memes may be nonsense, some of this variety may prove useful; in all these permutations, some “correct answers” may be hit upon. 

This is analogous to the biological process of mutation—most mutations are harmful or neutral, but, in the midst of the plethora of genetic variation is the occasional beneficial mutation, which confers adaptive value in specific challenging environments. Likewise, the Lilliputian far-right, subjected to stress under the repressive establishment Gulliver, undergoes varieties of memetic/ideological mutations, many useless or harmful, but several which may eventually allow the rightist organisms to flourish.

In the absence of this ideological diversity, one will find fewer “memetic mutations,” leaving the “movement” vulnerable to, and unable to adapt to, changing (perhaps more hostile) environments.  That’s one (of several) problems I have with the Alt Right – that this millennial marketing ploy seems intent on subsuming most of Der Movement within it, smothering what little memetic variability exists within a “movement” typically already characterized by rigid fossilized dogmas.  We need more ideological diversity now – a lot more – not less.  If we are all going to get our “Alt Right marching orders” from Pepe-Kek, mouthing empty platitudes about “God Emperor Trump” (and his Jewish family), it’s not going to go well with us at all.

Slime mold vs. rhizome should not be viewed as “either/or.”  Certainly, there will be periods that are (or should be) rhizome-predominant (like the present) and there will be (hopefully again in the future) slime mold-predominant periods.  But even at the height of slime mold organization and power, it would be prudent to retain some degree of rhizome structures – to have some groupuscules around, preserving memetic diversity, experimenting with new ideas, new ideologies, and novel ways of living and of interpreting sociopolitical realities. Better to have these alternative ideas and approaches on hand and easily accessible, in case they are required, than to face changing situations having to suddenly come up with ideological and/or strategic-tactical alternatives in a crisis. After a slime mold collapse, such as the collapse of fascism in 1945, it would be prudent to have at least some rhizomes around to “seed” the next ideological growth cycle.  Conversely, during the rhizome-predominant period, groupuscles should always at least attempt to strive toward developing to the slime mold level.  After all, the ultimate objective of the Sallis groupuscule is to make my ideas dominant within racial nationalism and then have a New Movement actualize those ideas through a revolutionary transformation of the White World (or what’s left of it).

Groupuscules for the sake of groupuscules is a sterile cul-de-sac, but a slime mold without any rhizome side growths risks being an evolutionary dead end.  And rhizomes that prematurely blossom into aborted slime mods, as seems to be happening now, can be a disaster.  Remember there is more to racial nationalism today than Alt Right-Pep-Kek-Trump and all the rest.

Shoup on Difference and the Emergence of Reality

Important theoretical science.

I want to give Bowery credit for alerting me to this important Shoup paper.

Sometimes, with the emphasis in science and technics in drilling down into highly specialized details of any given sub-sub-sub (etc.)-discipline, the bigger picture is disregarded.  Getting back to first principles and more fundamental understandings will likely yield important insights and discoveries, as I fear that an increasingly Judaized and Asianized science (it’s all about dem dere papers and grants) is causing us to miss the forest for the trees.

That’s science and technics.  With respect to racial activism, all the pseudo-philosophical blather that Majority Rights has degenerated into over the past several years does the opposite: obscures the fundamental necessitates of racial activism with abstract nonsense that is more “tree” than “forest.”  Der Movement is lost, completely adrift.

Getting back to Shoup: he asserts that difference is the ultimate foundation of reality; at their most fundamental level, objects (or any other entity) are defined by difference.

We can note the relevance to the concept of genetic interests, which is based on distinctive genetic information.  Hence, the greater the (genetic) difference, the greater are the (genetic) interests.  The greater the genetic difference (distance) between two biological entities, the greater the interest each entity has in its genetic continuity as contrasted to the other entity. Just as time and space emerges from the differences between objects, genetic interests emerge from the differences that exist between the information encoded in the DNA of biological entities.

Genetic Structure Redux

Genetic structure, from Western Biopolitics.

Something (slightly edited) from my old Western Biopolitics site about genetic structure, based on this paper, with a few new comments at the end.


Although this is highly preliminary, this is all completely consistent with what I (and James Bowery and Ben Tillman) have been saying for years: simple Fst measurements of genetic distance, while crucially important and necessary, are not sufficient to give the complete picture for EGI. Genetic distance based on structure is likely greater than that estimated from Fst for humans as well as for oak. Further, the genetic structure estimates can be viewed, as I’ve been saying, as an extra, independent measure of genetic distinctiveness superimposed on top of the foundation of Fst distance. Therefore, a complete estimation of EGI must include consideration of genetic structure, and this paper is an initial, preliminary attempt at quantifying that structure. More to come, we hope. This research groups compares analyses of combinations of coinherited alleles compared to the “one-by-one” Fst method. This paper is free online, take a close look at Table 1 – as the level of genetic structural complexity increases, genetic distance between the oak groups also increases. Note in all cases, emphasis added.

…is characterized by special combinations of genes. (To emphasize this aspect, genic integration might be the more appropriate term.) The main motivation for this paper was the realization that impacts of particular forces, selective or not, on population differentiation may not be observable at every level of genetic integration. Measurements of differentiation among populations based on gene frequencies, for example, provide no specific insights into the effects of mating systems nor of epistatic interaction on population differentiation. This is due to the fact that gene frequencies refer to the lowest level of genetic integration, namely its absence. This level, which is commonly addressed as a population’s gene-pool, is conceived to consist of the set of all individual genes present in the population members for a specified set of genetic traits. Genetic studies of population differentiation are almost always based on this “beanbag” (critically reflected by Mayr [2] and defended by Haldane [3]; for concise reasoning of the persistence of the gene-pool concept see e.g. [4] or [5]). Studies of differentiation at multiple loci are no exception, since they commonly report averages over single-locus differentiation indices. Also disregarded in studies of gene-pool differentiation are gene associations that deviate from Hardy-Weinberg proportions (homologous, or intralocus, association) or gametic equilibria (non-homologous, or interlocus, association). 

Considering that forms and degrees of gene association may differ at different levels of genetic integration, it thus appears that previous studies on patterns of population differentiation have provided very little information on levels of genetic integration above the gene-pool. One important reason for the usual focus on gene-pool differentiation is probably the lack of a method for measuring population differentiation consistently at all levels of genetic integration. Consistency means that comparison of the amount of differentiation among a set of populations between levels of integration provides information about the complexity of the gene associations that distinguish them. 

Since gene associations do not decrease as level of integration increase, neither should differentiation. Moreover, the extent of an increase in differentiation between subsequent levels should in some way reflect the degree of complexity of the additional gene associations, with equality as an indication of lack of additional complexity by some standard. Such a differentiation measure must thus be based on a conceptual characterization of the complexity of gene associations. The existence of such a measure would not only facilitate experimental studies… 

It turned out that the large increases in differentiation between levels that were observed in the real data were not producible in numerous simulations of simple selection models, indicating that these models cannot explain the complexity of the real data. 

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. 

Table 1 lists the distance matrix of pairwise distances…between stands and their mean as well as the symmetric population differentiation…SD and its components…j, both based on the elementary genic difference between genetic types, for each of three levels of integration: the gene-pool distance is the average of the six single-locus allelic distances; the single-locus diplophase distance is also the average over the loci; the multilocus diplophase distance. It is seen that for each pair of stands, all pairwise distances…increase considerably with the level of integration. 

Thus 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.


The authors then try to end the paper on a conservative, hedging note, perhaps to please reviewers:

This analysis is the first of its kind. Therefore, we cannot venture a prediction about whether the above findings on covariation between levels of integration constitute a general trend. It is conceivable, for example, that these findings are mainly determined by the conspicuously large polymorphism characteristic of the microsatellite markers used in this study. Other genetic markers may tell different stories.


Actually, there really is no logical reason to suppose that their findings are not generally applicable. It in fact makes perfect sense, as I (and others) have been arguing for years, that the correlation structure inherent in the genome is a general form of heritable genetic information above and beyond Fst, and that, therefore, this structure is an important part of genetic interests. There is no reason it must be limited to microsatellites; it is almost certainly an inherent, “emergent” characteristic of genetic information in all organisms. And, certainly, within and between human populations.


Therefore, it can be expected that genetic differentiation between human populations will be greater when overall structure (e.g., the combinations of coinherited alleles/genetic sequences) is considered, compared to Fst, and, that both Fst and genetic structure constitute genetic interests, both are important and both must be measured.


Genetic interests = Fst + Genetic Structure
And this paper is the initial step in the necessary quantification of genetic structure.
Yet more excerpts:

Conclusions: This new approach to the analysis of genetic differentiation among populations demonstrates that the consideration of gene associations within populations adds a new quality to studies on population differentiation that is overlooked when viewing only gene-pools. 

In general, traits are genetic only if they are inheritable, and the goal of inheritance analysis is to identify genes as the basic units of inheritance. The term genetic integration is used here to designate the combination or arrangement of these elementary objects “gene” into the haplotypes of gametes, into the genotypes at diploid (or polyploid) nuclei of diplophase individuals, or into the cytotypes of mitochondria or plastids, for example. 

At higher levels of genetic integration, where the objects of interest represent compositions of several individual genes together with their gene-types, association among gene-types becomes relevant for differentiation studies.

…neither the gene association within single loci (homologous association nor the gene association among loci (non-homologous association) is of the same form in any two stands, and in particular that association is present. Both the distances and the snail components show a much larger increase between the single-locus diplophase and the multilocus diplophase than between the gene-pool and the single-locus diplophase. 

Hence the non-homologous gene associations make a distinctly greater contribution to the differentiation than the homologous gene associations.

“Non-homologous gene associations” being a predominant component of what I refer to as “genetic structure.”


And consider the implications with respect for both EGI and parental kinship with intermarriage.


Genetic structure…here to stay.

New comments:

One question is whether the increase in genetic interests inherent between population (or individual) comparisons when taking genetic structure into account will be proportionately the same with increasing general genetic distance, or will the genetic structure differences increase proportionately with increasing genetic distance. For example, let’s hypothesize that genetic structure increases the genetic interest a Dane has with another Dane compared to a Greek by 50%, compared to allele-by-allele considerations. Will the increase in genetic interest of Dane vs. Nigerian also be 50%, or greater (it almost certainly could not be less). I hypothesize it would be greater, because the increase in allele-by-allele differences with greater genetic distance would lead to a proportionate increase in the genetic structure combination differences possible. Image ways of shuffling decks of cards where it is possible for the individual cards to differ between decks – the more individual card difference, the greater the number of novel card combinations between decks. This would of course need to be shown with the data (not that population geneticists would touch such a politically incorrect subject – they won’t even do genetic kinship studies). 
On a functional basis, one needs to consider epistasis. Certainly, there are cases where individual genes can influence phenotype; however, in the vast majority of cases, important phenotypic traits (the HBDers vaunted “form and function”) are affected by numbers of genes working together. This by the way is an important riposte to some of Dawkins’ more stupid extensions of his “selfish gene” meme, more properly, that should be plural, as in “selfish genes.” Or, perhaps, the “selfish genome.” In the end, selection acts upon the entire organism that is the product of all its (functional) genes. A given individual gene can of course affect the phenotype and influence that gene’s own selection, but even in that case, it does so in the context of the entire functional genome.
As I’ve written before, one cannot base genetic interests solely on “functional genes.” Putting aside that the distinction between functional and non-functional is becoming increasingly blurred due to findings that show that much of the “non-functional” genome actually does have function, the point is that even truly non-functional genes, if they vary in frequency between peoples, carry information on kinship and, even more to the point, as part of the distinctive genome, constitute a fraction of kinship, and thus have inherent value in this manner. After all, if genetic interests are based on genetic kinship, therefore all genes that constitute that kinship, as well as carry information that helps quantitate that kinship, have value. One can of course argue that functional genes that influence their own selection are of greater value on a “per gene” basis, but one cannot simply dismiss non-functional genes are being irrelevant to genetic interests.

Bowery’s Analysis of Salterian Genetic Investment

Another look at On Genetic Interests.

I have previously written on my perspectives about Salter’s genetic investment graphs from On Genetic Interests.  In the interests of giving credit where it is due, here I link to Bowery’s older post on the same topic which inspired my own analysis, and for which I recently remembered the name of the blog on which it is found..

I would like once again to take this opportunity to urge the reader – if they have not already done so – to obtain and read Salter’s book, a work that is unfortunately under-rated and ignored by Der Movement and also by serious nationalists in Europe.


Whither the Derb?

Not harsh enough.

To those who say “racial purists” are “too harsh” on Derbyshire, I say quite the opposite: not harsh enough.

Let’s consider the facts.  In the “feud” between Derbyshire and “purists,” Derb is more often than not the initiator, denouncing racialism, denouncing “purity,” promoting miscegenation,. criticizing racialist conference attendees, etc.  He constantly “trolls” using his own family as bait (nice character trait there).  He, not the “purists,” is the source of the problem.

When he was in mainstream conservatism, he routinely attacked KMacD, and promoted the idea (originally stated by someone probably a Jew) that Amren conference attendees were “latrine flies.”  But – lo and behold! – once the Derb gets kicked out of Conservatism, Inc. because of his juvenile “the talk” essay he went hat-in-hand to the same “purists” he previously denounced, and those people, bizarrely, welcomed him with open arms, and had Derbyshire speak at same conference that he previously mocked.

If that’s not enough, after being given this assistance by those he attacked, he continues to mock them! I mean, is this guy a low-life lousy bastard or what?  

There have been people I have debated online over the years, sometimes very vociferously, but some of them I can have respect for.  Bowery is an example.  I disagree with him more often than not, but one can have respect for his intellectual integrity.  Derbyshire on the other hand is really the lowest of the low, an ingrate, a hypocritical opportunist who constantly bites the hand that (literally in a sense) feeds him.

No, not harsh enough.

Giving Credit Where It is Due

Interesting.

Someone else came up with a diversity-autism theory several years ago, albeit somewhat different from my theory and without speculation of mechanism (apart from “pesticides”).  I don’t know if there is evidence of “sub-racial” mixing leading to increased autism (other than anecdotal evidence); however, on this blog we have already looked at evidence that mixed-race (at the continental level) individuals have higher autism rates.

Also, James Bowery has to be given credit for pointing out interesting correlations between autism rates in certain populations (e.g., Finns) and exposure to South Asians, although he favored an infectious pathogen theory for the mechanism, while I favor the amygdala and neural networks.