A second review of two papers.
Social Epistasis Amplifies the Fitness Costs of Deleterious Mutations, Engendering Rapid Fitness Decline Among Modernized Populations
June 2017Evolutionary Psychological Science 3(2)
DOI: 10.1007/s40806-017-0084-x
Michael Anthony Woodley of MenieMichael Anthony Woodley of MenieMatthew A. SarrafRadomir N. PestowHeitor B. F. FernandesHeitor B. F. Fernandes
Deleterious mutations are typically understood exclusively in terms of their harmful effects on carrier organisms. But there are convincing reasons to think that such adverse effects are not confined to the individual level. We argue that in social species, interorganismal gene-gene interactions, which in previous literatures have been termed social epistasis, allow genomes carrying deleterious mutations to reduce via group-level pleiotropy the fitness of others, including noncarriers. This fitness reduction occurs by way of degradation of group-level processes that optimize the reproductive ecology of a population for intergroup competition through, among other mechanisms, suppression of free-riding. Such damage to group regulatory processes suggests a hidden role for the accumulation of behavior-altering “spiteful” mutations in the dynamics of the demographic transition—these mutations may have contributed to the maladaptive outcomes of this process, such as widespread subreplacement fertility. A structured population model is presented describing aspects of this social epistasis amplification model. This phenomenon is also considered as a potential explanation for the results of Calhoun’s mouse utopia experiments, which provide an opportunity to directly test a major prediction stemming from the model.
I have mentioned this work before, but I would like to add additional commentary here. This new work is a re-review, an update, with some fresh perspectives.
Social epistasis describes gene-gene interactions between organisms, mediated by their phenotypes, or, more properly, extended phenotypes, the effects of which extend beyond the organism expressing that phenotype.
An example from the animal kingdom given by the authors is that of eusocial insects, where the size of members of the worker caste is influenced by the phenotypes of other castes. Thus, a genetically influenced trait – worker caste size – is affected by genetically influenced traits of other members of the broader group. The idea is that this occurs in humans and that relaxed natural selection (due to easier ecological conditions, technology, improved medical advances and hygiene, as well as ways of masking physical defects and unattractiveness – as well as a hyper-capitalist economy that rewards dark triad traits) among modern (Western) populations gives rise to a larger mutation load in the population, leading to aberrant phenotypes that negatively affect the fitness of the entire society. Thus, the genes of those with these spiteful mutations not only results in a maladaptive phenotype in those individuals, but, through social epistasis incurring negative influences in the society, spitefully reduces the (genetically influenced) fitness of others. Indeed, by altering the environment, the mutant unfit may create conditions that promote higher mutational loads in society at large, causing a dysgenic positive feedback loop. In such cases, mutational meltdown from the consequences of an excessive mutational load can occur. The demographic collapse of Western populations, coupled with replacement-level immigration (from populations less affected by these trends) may result from these processes, and thus social epistasis would have a devastating effect on the ethnic genetic interests of Western populations. In this sense, we observe the triumph of Bioleninism and the collapse of Western civilization. We can speculate if similar processes were linked to the collapse of previous civilizations that had relatively high standards of living and relaxed selection, such as the Classical. Genetic pacification and other influences of social epistasis may have made those societies easy prey for barbarians with lower mutational load and fewer social pathologies.
As the authors point out, in a healthy society, high status individuals would promote social cultural norms that enhance group fitness, such as ethnocentrism and the suppression of free riders. On the other hand, relaxed selection leads to high status individuals with spiteful mutations that produce behaviors that promote social abnormality and destructive cultural artifacts. Pathological altruism increases, ethnocentrism is pathologized, free riding is encouraged, and “clever silly” ideas are pushed into society with negative results.
From the “clever silly” paper:
My hunch is that it is this kind of IQ-advertisement which has led to the most intelligent people in modern societies having ideas about social phenomena that are not just randomly incorrect (due to inappropriately misapplying abstract analysis) but are systematically wrong. I am talking of the phenomenon known as political correctness (PC) in which foolish and false ideas have become moralistically-enforced among the ruling intellectual elite. And these ideas have invaded academic, political and social discourse. Because while the stereotypical nutty professor in the hard sciences is a brilliant scientist but silly about everything else; the stereotypical nutty professor social scientist or humanities professor is not just silly about ‘everything else’, but also silly in their professional work…The results of cognitive stratification and IQ-advertising are therefore bad enough to have destroyed the value of whole domains of the arts and academia, and in the domain of public policy the results have been simply disastrous. Over the past four decades the dishonest fantasy-world discourse of non-biological political correctness has evolved to dominate the intellectual arena of whole nations – perhaps the whole developed world – such that wrong and ridiculous ideas have become not just mainstream, but compulsory
Thus, narcissistic egoists, through extended phenotypes and social epistasis, lowers the fitness of society as a whole, causing the genetic representation of their ethny to decrease. Even more troubling, a positive feedback loop is established in that social epistasis allows for the behavior derived from spiteful selection to change the environment to select for the further accumulation of mutational load and selection for more egoist freaks. In the short term, it would seem like the botched now have an adaptive advantage but they do not for two major reasons. One, as mutational load increases and its consequent behavior spreads through the population, a threshold is reached in which mutational collapse and social collapse occurs. All sorts of social pathologies follow in the wake of spiteful mutations and social epistasis and the center will not hold. Second, and related to the first, populations not affected by these trends will continue to select for ethnocentric and more adaptively sound people, and in competition with the Bioleninist freaks, the more sound will win the game of adaptive fitness. Thus, any advantage the mutants may have via an altered advantage would be temporary. In the long run, over time, fitness collapses.
A model system by the authors demonstrates that the situation cane be stable only as long as the death rate among the mutants is high enough to sufficiently engage purifying selection against the misfits. This does not seem to be occurring and the situation is exacerbated by migration of populations lacking such spiteful mutations.
The authors make a connection between the human social epistasis situation and Calhoun’s rodent utopia experiments and they propose an experiment in which CRISPR-mediated genetic modification of genes known or suspected to control abnormal behaviors in Calhounian mice can be used to artificially purify the population and stabilize the situation. Understanding the entire social epistasis process is important since, as the authors state, the human situation is a “potentially significant threat.” One could also speculate positive social epistasis, where the genetically influenced extended phenotypes of some in the population enhanced societal fitness and promotes a more robust environment in which more adaptive genetic suites and the consequent traits are selected for. That is akin to the discussion by the authors of high status individuals lacking spiteful mutations promoting adaptive social norms. That is what should be aimed for.
One interesting point for my perspective is that social epistasis means that we may need to extend our understanding of ethnic genetic interests even further than genetic structure and genetic integration of individuals forming a population and then the results averaged over the population (or, in a similar vein, e.g. the consensus SNPs for a population being used). Perhaps the genepool of the entire population, taken together, with all if its interactions, needs to be considered as one suprapersonal entity, with multilocus genotypes extending over the entire ethny, co-adapted gene complexes being ethny-wide, and the genetic epistasis of the ethny feeding into social epistasis. We will need to consider the genetic integration, the structure, of the entire “ethnic’ genome, representing one giant organism (each ethny member being akin to one cell). This begins to fit in to my ethnotype idea, with a particular focus on those genes controlling the relevant extended phenotypes.
I can also speculate a memetic interpretation, in which fitness and reproduction is associated with numbers of recruits, followers, and supporters, and that mutational load can allude to memes as well as genes – although all of this can be ultimately linked to genetic social epistasis, since biologically defective egoists may be responsible for the negative memes occurring. In a dissent movement, narcissistic rent-seeking egoist grifters can alter the environment to satisfy their needs and to create a context in which destructive memes and other egoists thrive. This selects against honest, authentic, capable activists and their healthier memes. But just like the situation with genetic social epistasis, this seeming adaptive fitness of the Memetoleninist freaks is an illusion; it is temporary. As the memetic “mutational load” increases, collapse is ultimately inevitable, and particularly so when the movement comes up against competing systems and ideologies. The relevance to the Dissident Right should be obvious.
See this, which I discussed previously as well, but deserves re-mention. Emphasis added:
Abstract
Assessing the impact of the social environment on health and disease is challenging. As social effects are in part determined by the genetic makeup of social partners, they can be studied from associations between genotypes of one individual and phenotype of another (social genetic effects, SGE, also called indirect genetic effects). 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) contributes to variation in organismal and molecular measures related to anxiety, wound healing, immune function, and body weight. Social genetic effects explained up to 29% of phenotypic variance, and for several traits their contribution exceeded that of direct genetic effects (effects of an individual’s genotypes on its own phenotype). Importantly, we show that ignoring SGE can severely bias estimates of direct genetic effects (heritability). Thus SGE may be an important source of “missing heritability” in studies of complex traits in human populations. In summary, our study uncovers an important contribution of the social environment to phenotypic variation, sets the basis for using SGE to dissect social effects, and identifies an opportunity to improve studies of direct genetic effects.
Author Summary
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.
In both inbred and outbred mice, SGE influenced traits, particularly those related to “anxiety, wound healing, immune function, and body weight.” In some cases, changes in gene expression in the brain were observed.
If we extend these findings to humans, and further extend it to society-level interactions of population groups living in a defined territory, we are faced with the possibility with those we are forced to live amongst are, through SGE, changing our phenotype, via altered gene expression (and possibly through epigenetics and other effects). Consider the traits identified as strongly affected by SGE in the mouse study. Anxiety has wide-spread effects on human behavior and can explain many social pathologies extant today. Wound healing obviously has health-related effects, including, possibly, cancer. Immune function is of great importance, particularly in an era in which diversity, immigration, and globalism exposes us to novel pathogens. Body weight as a factor raises alarms about the obesity epidemic.
It is bad enough when this occurs as a result of exposure to, e.g., co-ethnic spiteful mutants, but even worse when enforced diversity via multiculturalism and mass migration exposes us to genetically alien peoples whose presence may be (negatively) affecting us at the level of genes, gene expression, and genetically-determined phenotypes. Our fundamental physical and behavioral being may be deformed, damaged, twisted, by diversity. It is paramount that we return to more homogeneous conditions that are congenial to our genetic-phenotypic well-being.
Further, these findings, particularly concerning behavior, is supportive of my thesis that increasing diversity is associated, in a causative manner, to high rates of autism observed in recent decades. The presence of genetically divergent human populations in the same territory can induce behavioral changes, and alteration in brain-specific gene expression, resulting in autism and other mental disorders (anxiety, depression, addiction, transgender and suicidal ideation) in vulnerable individuals. People concerned about autism perhaps should concentrate more on reducing diversity than on opposing vaccination.
In addition, SGE can result in overestimation of heritability estimates in twin studies, which may induce a nervous breakdown or two among the HBDers.
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