EGI Notes

Friday, March 17, 2017

Social Epistasis, Social Genetic Effects, and Harsh Reality

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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