Social epistasis amplification model

From Incel Wiki
Jump to navigation Jump to search

The social epistasis amplification model (SEAM) is the hypothesis that there exist harmful genetic mutations that damage not only the reproductive viability of the individual organisms which carry them, but that these mutations also reduce the overall fitness of the superorganism (in this case, human society) to which they belong, specifically via a feedback loop called social epistasis amplification, which ultimately involves these individual mutations degrading beneficial communal behaviors (that are argued to be mediated by social epistasis).

The carriers of these mutations that produce behaviors or characteristics that are detrimental to the carrier's overall fitness and others, are known as spiteful mutants in evolutionary biology.[1]

Social epistasis amplification is a purported process where the genotype of individuals carrying these 'spiteful mutations' disrupts the gene expression of non-mutated individuals via epistatic pathways, which is thought to lead to the prevalence of certain harmful and deviant behaviors and traits increasing rapidly in society as the increased social disruption increases the prevalence of deviant behaviors ever more, again via social epistasis. The authors of the theory even make dire predictions that this could potentially lead to a behavioral sink, meaning complete population collapse.

The main proponent of this theory, Dr. Michael A. Woodley of Menie, argued in a live stream that social epistasis amplification is possibly a major cause of the modern incel epidemic.[2]

Natural selection and mutation accumulation[edit | edit source]

The main author of SEAM, the prominent (and controversial) intelligence researcher Dr. Michael A. Woodley of Menie, argues that reduced natural selection pressure and the overall milder ecology of modern society, chiefly enabled by breakthroughs of the industrial revolution and modern medicine, have resulted in the fitness cost of deleterious mutations decreasing. He points out that pre-modernity, only 40% of people could fully participate in reproduction due to both pre- and postnatal infant mortality rates being high,[3] violent deaths being frequent,[4], the disease burden being much higher compared to the total world population at the time,[5] and a possible reduction in proportionate deaths by intra and inter-group violence (though the latter assertion is still somewhat controversial).

The formally harsher selection pressures meant that there used to be much greater purifying selection, in that a much smaller group of people had a disproportionate amount of offspring which resulted in a purging of deleterious mutations from the genome each generation. Carriers of deleterious mutations, on the other hand, had a reduced likelihood of successfully competing for scarce resources, a greater child mortality, and a their greater susceptibility to disease. (These arguments are related to the good genes hypothesis in which recognizable traits such as susceptibility to disease are assumed to be reliable indicators of overall genetic viability, i.e. a general fitness factor, which may in part be determined by overall mutational load due to pleiotropy, meaning that a single gene can affect multiple phenotypic features, including features like immunocompetence.)

Woodley of Menie argues, that spiteful mutations in particular can steadily increase in the population with the relaxation of natural selection pressures and disrupt the adaptive social or eusocial behavior of a species.

Mechanism[edit | edit source]

Epistasis is a well-researched genetic phenomenon in which genes affect the expression of a gene at another genetic locus (the place that a gene occupies on a chromosome). Woodley of Menie suggests that spiteful mutations pertaining to adaptive social behavior may disturb the gene expression of non-carriers of said mutations via social epistasis, meaning that genes from one organism affect the expression of genes in a social partner.

Social epistasis, or rather eusocial epistasis, has been proven to exist in certain types of eusocial insects, such as bees,[6] wherein the individual bee's (behavioral and non-behavioral) phenotype is affected by the overall genotypic composition of the colony. It appears the proper development of individual bees depends on the overall 'genetic' health of the hive with individual traits being partly mediated by social interactions between individual bees.

This idea brings to mind some Victoria era thinkers who perhaps anticipated this theory, and Nikola Tesla, who often compared human societies to eusocial insects such as bees.

In regards to humans, it is argued that these deleterious mutations combined with social epistatic effects lead to these 'spiteful mutants' sometimes reaching positions of social influence, as deleterious mutation accumulation might enable exceptional abilities to game the system's selection mechanisms, and certain traits generally associated with higher social status, such as intelligence are also only weakly linked to deleterious mutation accumulation.[7]

It is claimed that these 'spiteful mutants' then use their positions of power and influence to lead others to behave in ways that would have possibly have been highly maladaptive throughout humanity's evolutionary past by promoting the adoption of certain ideals, such as anti-natalism, atheism, and multiculturalism. They authors of the theory argue these ideals generally serve to inhibit fertility, a tautological statement in the case of anti-natalism.

Behavioral sink[edit | edit source]

Woodley draws on the theory of social epistasis amplification to explain the outcome of John C. Calhoun's famous rat utopia experiment.[8]

He argues that the 'behavioral sink,' i.e., the gradual and eventually complete breakdown of collective behavior and reproduction among the rodents in most of Calhoun's experiments, was mediated chiefly by 'spiteful mutant' mice carrying deleterious genes that served to disrupt social hierarchies and communal behavior via dysfunctional pheromone signals.

Woodley also asserts that similar mechanisms are at play in many modern societies, and claims that the low fertility rates in many modern societies, starting in most Western countries from the later midpoint of the 20th century onwards, are chiefly driven by the phenomenon of social epistasis amplification.[9]

Evidence for the hypothesis[edit | edit source]

Most of the evidence the SEAM authors point to corroborate their theory is indirect, owing to the obvious ethical difficulties of deliberately inducing deleterious mutations in a human research subject. Evidence that has been presented so far includes the fact that greater paternal age at birth is linked to lower levels of church attendance in individuals born after, but not before the 1960s[10] (indicating that the social epistasis amplification reached an inflection point around that date) that the heritability of the age of sexual debut has increased after the sexual revolution (ibid), the fact that 'psychopathic deviance' and mental illness has starkly increased in the population, particular in more modernized countries,[11] among other things.

All these lines of evidence point to a general decrease in group regulatory mechanisms suppressing 'free riders' (selfish individuals who do not contribute to the group's benefit) and an overall shift in society from goals related to group cohesion and mutual aid (religion, community, ethnocentrism, group affiliation) towards individualism, status drive and other motivations that focus more on the benefit of the individual in contrast to the good of the group.

However, this purported evidence does not prove that these purported social epistatic gene transfer effects play a large or even any role in this general breakdown of behavior that is adaptive on an individual and group level.

Woodley himself, while emphasizing that the SEAM is still highly theoretical, claims direct empirical evidence of this model has arrived via studies on mice, where the researchers found that mice with a 'mutation related to autistic-like behaviors' were observed to alter the behavior of other mice, lower their testosterone levels, and undermine the stability of their social hierarchies via social epistatic epigenetic effects, that seemingly resulted from mere contact with the mutated mice.

A team of researchers found that the mutant mice were secreting a pheromone called Darcin that resulted in the modification of the behavior of exposed healthy mice and that the social withdrawal-related behaviors of the mutated mice were independent of their environment, implying that Calhoun was incorrect when he claimed that the social withdrawal observed among the 'beautiful ones' in his famous experiment was due to overpopulation.[12] Woodley speculates that similar processes are playing out in contemporary human populations today.[13]

Criticism[edit | edit source]

Firstly, the model rests on the claim that group selection pressures have, or do operate on human genes throughout history in a significant manner, a claim that has been hotly disputed.[14]

Proponents of group selection argue that less sophisticated group selectionist arguments that have been debunked are no longer relevant and that selection operates on multiple levels concurrently, that is, at the level of the gene, the individual, the kin, and the group as a whole. That is, it can be both evolutionary adaptive to behave 'selfishly' within groups (assuming the group does not adequately check these free-riders), but also that highly altruistic, co-operative groups tend to triumph above others during periods of harsh group selection (such as competition over scarce resources, land, and violent conflicts).[15]

Different from eusocial species (in which social epistasis has been confirmed), humans do not occupy strict functional positions within the collective. Instead, there is substantial cultural variability and people are able to re-adapt to changing environments and new social functions in a highly general manner. Humans also exhibit a high robustness in behavioral development to moderate psychological trauma. It thus seems unlikely for some spiteful mutants to impact overall social behavior at all.

Other's have criticized Woodley's research on methodological and theoretical grounds, A team of researchers made a reply to one of Woodley's papers citing them, claiming that Woodley had misrepresented their work. They argued his work claiming relaxed mutation-selection leading to catastrophic increases in deleterious mutations in the general population was alarmist in nature. They also claim that purifying selection still operates to a high level in modern society, and that current levels of mutational load are not historically unprecedented.

The authors argued that Woodley's claim that contemporary populations had very high mutational load was based on several dubious assumptions. These assumptions include that people were generally mutation free before the Industrial Revolution, population size was always constant, and generation times were fixed and short. They also claimed Woodley put too much of an overall greater focus on natural selection pressures (viability), disregarding sexual selection pressures.

They argue that such arguments frequently discard human-driven behaviors that alter the mutation-selection balance such as reduced rates of inbreeding, pre-natal selection (abortion), and sexual selection against deleterious mutations.[16]

References[edit | edit source]

See also[edit | edit source]



Biological essentialismEugenicsAnti-EnvironmentalismTraditionalist conservatismFatalismBlackpillScientific BlackpillScientific Blackpill (Supplemental)Behavioral sinkHypergamyMatthew effectBeautyFisherian runawayGood genes hypothesisDominance hierarchyIntrasexual competitionJ. D. UnwinSexual sublimationFemale subordinationOnline datingPhysiognomyPersonality


SlutMonogamyMarriageArranged marriagePolygynyPolyandry



BlackpillRacepillHeightpillDickpillBaldpillShitpillDogpillBirdpillTeen love pill

It's over

Cope or ropeCopeRopingLay down and rotInbreeding depressionOutbreeding depressionMutationSocial epistasis amplification modelAtavismReproductive successDemographics of inceldomCauses of inceldomAdverse effects of inceldomEvolutionary mismatchBehavioral sinkRegression toward the meanPeaked in high schoolFOMOSexual envy