nhaliday + perturbation   31

What are the Laws of Biology?
The core finding of systems biology is that only a very small subset of possible network motifs is actually used and that these motifs recur in all kinds of different systems, from transcriptional to biochemical to neural networks. This is because only those arrangements of interactions effectively perform some useful operation, which underlies some necessary function at a cellular or organismal level. There are different arrangements for input summation, input comparison, integration over time, high-pass or low-pass filtering, negative auto-regulation, coincidence detection, periodic oscillation, bistability, rapid onset response, rapid offset response, turning a graded signal into a sharp pulse or boundary, and so on, and so on.

These are all familiar concepts and designs in engineering and computing, with well-known properties. In living organisms there is one other general property that the designs must satisfy: robustness. They have to work with noisy components, at a scale that’s highly susceptible to thermal noise and environmental perturbations. Of the subset of designs that perform some operation, only a much smaller subset will do it robustly enough to be useful in a living organism. That is, they can still perform their particular functions in the face of noisy or fluctuating inputs or variation in the number of components constituting the elements of the network itself.
scitariat  reflection  proposal  ideas  thinking  conceptual-vocab  lens  bio  complex-systems  selection  evolution  flux-stasis  network-structure  structure  composition-decomposition  IEEE  robust  signal-noise  perturbation  interdisciplinary  graphs  circuits  🌞  big-picture  hi-order-bits  nibble  synthesis 
november 2017 by nhaliday
What Does a “Normal” Human Genome Look Like? | Science
So, what have our first glimpses of variation in the genomes of generally healthy people taught us? First, balancing selection, the evolutionary process that favors genetic diversification rather than the fixation of a single “best” variant, appears to play a minor role outside the immune system. Local adaptation, which accounts for variation in traits such as pigmentation, dietary specialization, and susceptibility to particular pathogens is also a second-tier player. What is on the top tier? Increasingly, the answer appears to be mutations that are “deleterious” by biochemical or standard evolutionary criteria. These mutations, as has long been appreciated, overwhelmingly make up the most abundant form of nonneutral variation in all genomes. A model for human genetic individuality is emerging in which there actually is a “wild-type” human genome—one in which most genes exist in an evolutionarily optimized form. There just are no “wild-type” humans: We each fall short of this Platonic ideal in our own distinctive ways.
article  essay  org:nat  🌞  bio  biodet  genetics  genomics  mutation  genetic-load  QTL  evolution  sapiens  survey  summary  coding-theory  enhancement  signal-noise  egalitarianism-hierarchy  selection  tradeoffs  immune  recent-selection  perturbation  nibble  ideas  forms-instances 
november 2017 by nhaliday
Stability of the Solar System - Wikipedia
The stability of the Solar System is a subject of much inquiry in astronomy. Though the planets have been stable when historically observed, and will be in the short term, their weak gravitational effects on one another can add up in unpredictable ways. For this reason (among others) the Solar System is chaotic,[1] and even the most precise long-term models for the orbital motion of the Solar System are not valid over more than a few tens of millions of years.[2]

The Solar System is stable in human terms, and far beyond, given that it is unlikely any of the planets will collide with each other or be ejected from the system in the next few billion years,[3] and the Earth's orbit will be relatively stable.[4]

Since Newton's law of gravitation (1687), mathematicians and astronomers (such as Laplace, Lagrange, Gauss, Poincaré, Kolmogorov, Vladimir Arnold and Jürgen Moser) have searched for evidence for the stability of the planetary motions, and this quest led to many mathematical developments, and several successive 'proofs' of stability of the Solar System.[5]


The planets' orbits are chaotic over longer timescales, such that the whole Solar System possesses a Lyapunov time in the range of 2–230 million years.[3] In all cases this means that the position of a planet along its orbit ultimately becomes impossible to predict with any certainty (so, for example, the timing of winter and summer become uncertain), but in some cases the orbits themselves may change dramatically. Such chaos manifests most strongly as changes in eccentricity, with some planets' orbits becoming significantly more—or less—elliptical.[7]

Is the Solar System Stable?: https://www.ias.edu/ideas/2011/tremaine-solar-system

Is the Solar System Stable?: https://arxiv.org/abs/1209.5996
nibble  wiki  reference  article  physics  mechanics  space  gravity  flux-stasis  uncertainty  robust  perturbation  math  dynamical  math.DS  volo-avolo  multi  org:edu  org:inst  papers  preprint  time  data  org:mat 
november 2017 by nhaliday
How to Escape Saddle Points Efficiently – Off the convex path
A core, emerging problem in nonconvex optimization involves the escape of saddle points. While recent research has shown that gradient descent (GD) generically escapes saddle points asymptotically (see Rong Ge’s and Ben Recht’s blog posts), the critical open problem is one of efficiency — is GD able to move past saddle points quickly, or can it be slowed down significantly? How does the rate of escape scale with the ambient dimensionality? In this post, we describe our recent work with Rong Ge, Praneeth Netrapalli and Sham Kakade, that provides the first provable positive answer to the efficiency question, showing that, rather surprisingly, GD augmented with suitable perturbations escapes saddle points efficiently; indeed, in terms of rate and dimension dependence it is almost as if the saddle points aren’t there!
acmtariat  org:bleg  nibble  liner-notes  machine-learning  acm  optimization  gradient-descent  local-global  off-convex  time-complexity  random  perturbation  michael-jordan  iterative-methods  research  learning-theory  math.DS  iteration-recursion 
july 2017 by nhaliday
Is Pharma Research Worse Than Chance? | Slate Star Codex
Here’s one hypothesis: at the highest level, the brain doesn’t have that many variables to affect, or all the variables are connected. If you smack the brain really really hard in some direction or other, you will probably treat some psychiatric disease. Drugs of abuse are ones that smack the brain really hard in some direction or other. They do something. So find the psychiatric illness that’s treated by smacking the brain in that direction, and you’re good.

Actual carefully-researched psychiatric drugs are exquisitely selected for having few side effects. The goal is something like an SSRI – mild stomach discomfort, some problems having sex, but overall you can be on them forever and barely notice their existence. In the grand scheme of things their side effects are tiny – in most placebo-controlled studies, people have a really hard time telling whether they’re in the experimental or the placebo group.


But given that we’re all very excited to learn about ketamine and MDMA, and given that if their original promise survives further testing we will consider them great discoveries, it suggests we chose the wrong part of the tradeoff curve. Or at least it suggests a different way of framing that tradeoff curve. A drug that makes you feel extreme side effects for a few hours – but also has very strong and lasting treatment effects – is better than a drug with few side effects and weaker treatment effects. That suggests a new direction pharmaceutical companies might take: look for the chemicals that have the strongest and wackiest effects on the human mind. Then see if any of them also treat some disease.

I think this is impossible with current incentives. There’s too little risk-tolerance at every stage in the system. But if everyone rallied around the idea, it might be that trying the top hundred craziest things Alexander Shulgin dreamed up on whatever your rat model is would be orders of magnitude more productive than whatever people are doing now.
ratty  yvain  ssc  reflection  psychiatry  medicine  pharma  drugs  error  efficiency  random  meta:medicine  flexibility  outcome-risk  incentives  stagnation  innovation  low-hanging  tradeoffs  realness  perturbation  degrees-of-freedom  volo-avolo  null-result 
june 2017 by nhaliday
Polymorphisms and Load | West Hunter
Anyhow, we now have some estimates of the relative influence of common variants on various traits (from recent Visscher-type papers) . The fraction of genetic variation that can be explained by common variants is about half for height and IQ, one-third for schizophrenia, one-quarter for BMI, and about one-fifth for personality, as measured by standard personality measures, which I don’t have much faith in. If I had to guess, and at this point I do, the more that trait variation is a deviation from the selective optimum, rather than being orthogonal to fitness, the more it is influenced by load.
west-hunter  scitariat  discussion  biodet  behavioral-gen  genetics  QTL  population-genetics  genetic-load  data  iq  embodied  psychiatry  personality  stylized-facts  prediction  variance-components  correlation  evolution  sapiens  mutation  distribution  🌞  disease  health  fitness  psychology  cog-psych  spearhead  perturbation 
may 2017 by nhaliday
Social Epistasis Amplifies the Fitness Costs of Deleterious Mutations, Engendering Rapid Fitness Decline Among Modernized Populations | SpringerLink
- Michael A. Woodley

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.


Fitness indicators theory (Houle 2000; Miller 2000) predicts that the behavioral and physiological condition of prospective partners strongly influences female mate choice in particular, as these constitute honest indicators of underlying genetic quality. Furthermore, as deleterious mutations are pleiotropic (i.e., they can influence the development of multiple traits simultaneously), they are a source of genetic correlation among diverse behavioral and physiological domains, yielding a latent general fitness factor( f ). This optimizes the efficiency of sexual selection, as selection for quality with respect to one domain will increase the probability of selection for quality “across the board” (Houle 2000; Miller 2000). If purifying selection is primarily cryptic—working by virtue of those lower in f simply being less successful in competition for mates and therefore producing fewer offspring relative to those higher in the factor—then considerably less reproductive failure is needed to solve the mutation load paradox (19% instead of 88% based on simulations in Leseque et al. 2012).


Theoretical work involving humans suggests a loss of intrinsic fitness of around 1% per generation in the populations of modernized countries (Lynch 2016; Muller 1950). Thus, these might yet be undergoing mutational meltdown, albeit very gradually (i.e., over the course of centuries)


An interesting observation is that the fitness of the populations of modernized nations does appear to be rapidly decreasing—although not in a manner consonant with the direct action of deleterious mutations on the fitness of individuals (as per the mutation load paradox).


Increased education has furthermore encouraged individuals to trade fertility against opportunities to enhance their social status and earning power, with the largest fitness losses occurring among those with high status who potentially carry fewer deleterious mutations (i.e., by virtue of possessing higher levels of traits that exhibit some sensitivity to mutation load, such as general intelligence; Spain et al. 2015; Woodley of Menie et al. 2016a). Hitherto not considered is the possibility that the demographic transition represents a potential change in the fitness characteristics of the group-level extended phenotype of modernized populations, indicating that there might exist pathways through which deleterious mutations that accumulate due to ecological mildness could pathologically alter fertility tradeoffs in ways that might account for the maladaptive aspects of the fertility transition (e.g., subreplacement fertility; Basten, Lutz and Scherbov, 2013).


Cooperation, though offering significant fitness benefits to individual organisms and groups, involves some costs for cooperators in order to realize mutual gains for all parties. Free riders are individuals that benefit from cooperation without suffering any of the costs needed to sustain it. Hence, free riders enjoy a fitness advantage relative to cooperators via the former’s parasitism on the latter.


The balance of selection can alternate between the different levels depending on the sorts of selective challenges that a population encounters. For example, group selection may operate on human populations during times of intergroup conflict (i.e., warfare), whereas during times of peace, selection may tend to favor the fitness of individuals instead (Woodley and Figueredo 2013; Wilson 2002). A major factor that seems to permit group-level selection to be viable under certain ecological regimes is the existence of free-rider controls, i.e., features of the group’s social ecology that curb the reproductive fitness of the carriers of “selfish” genetic variants (MacDonald 1994; Wilson 2002).


High-status individuals participate in the generation and vertical cultural transmission of free-rider controls—these take the form of religious and ideological systems which make a virtue out of behaviors that overtly benefit the group, and a vice out of those that only favor individual-level fitness, via the promotion of ethnocentrism, martyrdom, and displays of commitment (MacDonald 1994, 2009, 2010; Wilson 2002). Humans are furthermore equipped with specialized mental adaptations for coordinating as part of a group, such as effortful control—the ability to override implicit behavioral drives via the use of explicit processing systems, which allow them to regulate their behavior based on what is optimal for the group (MacDonald 2008). The interaction between individuals of different degrees of status, i.e., those that generate and maintain cultural norms and those who are merely subject to them, therefore constitutes a form of social epistasis, as the complex patterns of interactions among genomes that characterize human culture have the effect of regulating both individual- and group-level (via the curbing of free-riding) fitness (MacDonald 2009, 2010).

Mutations that push the behavior of high-status individuals away from the promotion of group-selected norms may promote a breakdown of or otherwise alter these social epistatic interactions, causing dysregulation of the group’s reproductive ecology. Behavioral changes are furthermore a highly likely consequence of mutation accumulation, as “behavior” (construed broadly) is a large potential target for new mutations (Miller 2000; Lynch 2016) 1 owing to the fact that approximately 84% of all genes in the human genome are involved in some aspect of brain development and/or maintenance (Hawrylycz et al. 2012).

Consistent with the theorized role of group-level (cultural) regulatory processes in the maintenance of fitness optima, positive correlations exist between religiosity (a major freerider control; MacDonald 1994; Wilson 2002) and fertility, both at the individual differences and cross-cultural levels (Meisenberg 2011). Religiosity has declined in modernized nations—a process that has gone hand-in-hand with the rise of a values system called postmaterialism (Inglehart 1977), which is characterized by the proliferation of individualistic, secular, and antihierarchical values (Welzel 2013). The holding of these values is negatively associated with fertility, both at the individual level (when measured as political liberalism; Goldstone et al. 2011) and across time and cultures (Inglehart and Appel 1989). The rise of postmaterialist values is also associated with increasingly delayed onset of reproduction (Klien 1990) which directly increases the (population) mutation load.

Pathological Altruism

Some of the values embodied in postmaterialism have been linked to the pathological altruism phenomenon, i.e., forms of altruism that damage the intended recipients or givers of largesse (Oakley et al. 2012; Oakley 2013). Virtues associated with altruism such as kindness, fidelity, magnanimity, and heroism, along with quasi-moral traits associated with personality and mental health, may be under sexual selection and might therefore be sensitive, through the f factor, to the deleterious effects of accumulating mutations (Miller 2007).


Another form of pathologically altruistic behavior that Oakley (2013) documents is self-righteousness, which may be increasing, consistent with secular trend data indicating elevated levels of self-regarding behavior among Western populations (sometimes called the narcissism epidemic; Twenge and Campbell 2009). This sort of behavior constitutes a key component of the clever silly phenomenon in which the embrace of counterfactual beliefs is used to leverage social status via virtue signaling (e.g., the conflation of moral equality among individuals, sexes, and populations with biological equality) (Dutton and van der Linden 2015; Charlton 2009; Woodley 2010). There may be a greater number of influential persons inclined to disseminate such beliefs, in that the prevalence of phenotypes disposed toward egoistic behaviors may have increased in Western populations (per Twenge and coworkers’ research), and because egoists, specifically Machiavellians and narcissists, appear advantaged in the acquisition of elite societal stations (Spurk et al. 2015).

[Do Bad Guys Get Ahead or Fall Behind? Relationships of the Dark Triad of Personality With Objective and Subjective Career Success: http://sci-hub.tw/http://journals.sagepub.com/doi/abs/10.1177/1948550615609735

After controlling for other relevant variables (i.e., gender, age, job tenure, organization size, education, and work hours), narcissism was positively related to salary, Machiavellianism was positively related to leadership position and career satisfaction, and psychopathy was negatively related to all analyzed outcomes.]


By altering cultural norms, elite egoists may encourage the efflorescence of selfish behaviors against which some older and once highly influential cultural systems acted. For example, Christianity in various forms strongly promoted personal sacrifice for the good of groups and proscribed egoistic behaviors (Rubin 2015), but has declined significantly in terms of cultural power following modernization (Inglehart 1977). Thus, it is possible that a feedback loop exists wherein deleterious mutation accumulation raises population levels of egoism, either directly or indirectly, via the breakdown of developmental constraints on personality canalization; the resultantly greater number of egoists are then able to exploit relevant personality traits to attain positions of sociocultural influence; and through these … [more]
study  speculation  models  biodet  bio  sapiens  evolution  genetic-load  paternal-age  the-monster  slippery-slope  society  social-structure  free-riding  coordination  EGT  dynamical  🌞  fertility  dysgenics  eh  self-control  obesity  altruism  mutation  multi  twitter  social  commentary  perturbation  gnon  new-religion  science-anxiety  population-genetics  biophysical-econ  hmm  discipline  autism  scitariat  clown-world  epidemiology  malaise  sociology  demographic-transition  blowhards  model-organism  nonlinearity  civilization  expression-survival  universalism-particularism  order-disorder  trends  deep-materialism  values  ideology  domestication  cohesion  christopher-lasch  scale  patho-altruism  social-capital  behavioral-gen  madisonian  chart  nihil  aristos  piracy  theos  cultural-dynamics  roots  zeitgeist  rot  the-bones  counter-revolution  pdf  modernity  microfoundations  video  presentation  religion  christianity  health  longevity  ethnocentrism  genetic-correlation  👽  instinct 
march 2017 by nhaliday
Neurodiversity | West Hunter
Having an accurate evaluation of a syndrome as a generally bad thing isn’t equivalent to attacking those with that syndrome. Being a leper is a bad thing, not just another wonderful flavor of humanity [insert hot tub joke] , but that doesn’t mean that we have to spend our spare time playing practical jokes on lepers, tempting though that is.. Leper hockey. We can cure leprosy, and we are right to do so. Preventing deafness through rubella vaccination was the right thing too – deafness sucks. And so on. As we get better at treating and preventing, humans are going to get more uniform – and that’s a good thing. Back to normalcy!

focus: https://westhunt.wordpress.com/2017/02/22/neurodiversity/#comment-88691
interesting discussion of mutational load: https://westhunt.wordpress.com/2017/02/22/neurodiversity/#comment-88793

I was thinking again about the consequences of having more small-effect deleterious mutations than average. I don’t think that they would push hard in a particular direction in phenotype space – I don’t believe they would make you look weird, but by definition they would be bad for you, reduce fitness. I remembered a passage in a book by Steve Stirling, in which our heroine felt as if her brain ‘was moving like a mechanism of jewels and steel precisely formed.’ It strikes me that a person with an extra dollop of this kind of genetic load wouldn’t feel like that. And of course that heroine did have low genetic load, being the product of millennia of selective breeding, not to mention an extra boost from the Invisible Crown.

Well, what does the distribution of fitness burden by frequency look like for deleterious mutations of a given fitness penalty?
It’s proportional to the mutation rate for that class. There is reason to believe that there are more ways to moderately or slightly screw up a protein than to really ruin it, which indicates that mild mutations make up most load in protein-coding sequences. More of the genome is made up of conserved regulatory sequences, but mutations there probably have even milder effects, since few mutations in non-coding sequences cause a serious Mendelian disease.

I have wondered if there was some sort of evolutionary tradeoff between muscles and brains over the past hundred thousand years through dystrophin’s dual role. There is some evidence of recent positive selection among proteins that interact with dystrophin, such as DTNBP1 and DTNA.

Any novel environment where higher intelligence can accrue more caloric energy than brute strength alone (see: the invention of the bow) should relax the selection pressure for muscularity. The Neanderthals didn’t fare so well with the brute strength strategy.
Sure: that’s what you might call an inevitable tradeoff, a consequence of the laws of physics. Just as big guys need more food. But because of the way our biochemistry is wired, there can be tradeoffs that exist but are not inevitable consequences of the laws of physics – particularly likely when a gene has two fairly different functions, as they often do.
west-hunter  discussion  morality  philosophy  evolution  sapiens  psychology  psychiatry  disease  neuro  scitariat  ideology  rhetoric  diversity  prudence  genetic-load  autism  focus  👽  multi  poast  mutation  equilibrium  scifi-fantasy  rant  🌞  paternal-age  perturbation  nibble  ideas  iq  quotes  aphorism  enhancement  signal-noise  blowhards  dysgenics  data  distribution  objektbuch  tradeoffs  embodied  speculation  metabolic  volo-avolo  degrees-of-freedom  race  africa  genetics  genomics  bio  QTL  population-genetics  stylized-facts  britain  history  early-modern  pre-ww2  galton  old-anglo  giants  industrial-revolution  neuro-nitgrit  recent-selection  selection  medicine  darwinian  strategy  egalitarianism-hierarchy  CRISPR  biotech  definition  reflection  poetry  deep-materialism  EGT  discrimination  conceptual-vocab 
february 2017 by nhaliday
The infinitesimal model | bioRxiv
Our focus here is on the infinitesimal model. In this model, one or several quantitative traits are described as the sum of a genetic and a non-genetic component, the first being distributed as a normal random variable centred at the average of the parental genetic components, and with a variance independent of the parental traits. We first review the long history of the infinitesimal model in quantitative genetics. Then we provide a definition of the model at the phenotypic level in terms of individual trait values and relationships between individuals, but including different evolutionary processes: genetic drift, recombination, selection, mutation, population structure, ... We give a range of examples of its application to evolutionary questions related to stabilising selection, assortative mating, effective population size and response to selection, habitat preference and speciation. We provide a mathematical justification of the model as the limit as the number M of underlying loci tends to infinity of a model with Mendelian inheritance, mutation and environmental noise, when the genetic component of the trait is purely additive. We also show how the model generalises to include epistatic effects. In each case, by conditioning on the pedigree relating individuals in the population, we incorporate arbitrary selection and population structure. We suppose that we can observe the pedigree up to the present generation, together with all the ancestral traits, and we show, in particular, that the genetic components of the individual trait values in the current generation are indeed normally distributed with a variance independent of ancestral traits, up to an error of order M^{-1/2}. Simulations suggest that in particular cases the convergence may be as fast as 1/M.

published version:
The infinitesimal model: Definition, derivation, and implications: https://sci-hub.tw/10.1016/j.tpb.2017.06.001

Commentary: Fisher’s infinitesimal model: A story for the ages: http://www.sciencedirect.com/science/article/pii/S0040580917301508?via%3Dihub
This commentary distinguishes three nested approximations, referred to as “infinitesimal genetics,” “Gaussian descendants” and “Gaussian population,” each plausibly called “the infinitesimal model.” The first and most basic is Fisher’s “infinitesimal” approximation of the underlying genetics – namely, many loci, each making a small contribution to the total variance. As Barton et al. (2017) show, in the limit as the number of loci increases (with enough additivity), the distribution of genotypic values for descendants approaches a multivariate Gaussian, whose variance–covariance structure depends only on the relatedness, not the phenotypes, of the parents (or whether their population experiences selection or other processes such as mutation and migration). Barton et al. (2017) call this rigorously defensible “Gaussian descendants” approximation “the infinitesimal model.” However, it is widely assumed that Fisher’s genetic assumptions yield another Gaussian approximation, in which the distribution of breeding values in a population follows a Gaussian — even if the population is subject to non-Gaussian selection. This third “Gaussian population” approximation, is also described as the “infinitesimal model.” Unlike the “Gaussian descendants” approximation, this third approximation cannot be rigorously justified, except in a weak-selection limit, even for a purely additive model. Nevertheless, it underlies the two most widely used descriptions of selection-induced changes in trait means and genetic variances, the “breeder’s equation” and the “Bulmer effect.” Future generations may understand why the “infinitesimal model” provides such useful approximations in the face of epistasis, linkage, linkage disequilibrium and strong selection.
study  exposition  bio  evolution  population-genetics  genetics  methodology  QTL  preprint  models  unit  len:long  nibble  linearity  nonlinearity  concentration-of-measure  limits  applications  🌞  biodet  oscillation  fisher  perturbation  stylized-facts  chart  ideas  article  pop-structure  multi  pdf  piracy  intricacy  map-territory  kinship  distribution  simulation  ground-up  linear-models  applicability-prereqs  bioinformatics 
january 2017 by nhaliday
Fluctuating Asymmetry and Environmental Stress: Understanding the Role of Trait History
A conceptually important source of heterogeneity in relationships with FA is variation in the selection history of the trait(s) under study, i.e. traits that experienced a (recent) history of directional change are predicted to be developmentally less stable, potentially through the loss of canalizing modifiers.
study  nature  evolution  developmental  robust  bio  biodet  oscillation  perturbation  roots 
january 2017 by nhaliday
J. Intell. | Free Full-Text | Zeroing in on the Genetics of Intelligence
Rare variants and mutations of large effect do not appear to play a main role beyond intellectual disability. Common variants can account for about half the heritability of intelligence and show promise that collaborative efforts will identify more causal genetic variants. Gene–gene interactions may explain some of the remainder, but are only starting to be tapped. Evolutionarily, stabilizing selection and selective (near)-neutrality are consistent with the facts known so far.

Idiot Proof: https://westhunt.wordpress.com/2016/01/07/idiot-proof/
I was looking at a recent survey of current knowledge in psychological genetics. The gist is that common variants – which can’t have decreased fitness much in the average past, since they’re common – are the main story in the genetic architecture of intelligence. Genetic load doesn’t seem very important, except at the low end. Big-effect deleterious mutations can certainly leave you retarded, but moderate differences in the number of slightly-deleterious mutations don’t have any observable effect – except possibly in the extremely intelligent, but that’s uncertain at this point. Not what I expected, but that’s how things look right now. It would seem that brain development is robust to small tweaks, although there must be some limit. The results with older fathers apparently fit this pattern: they have more kids with something seriously wrong, but although there should be extra mild mutations in their kids as well as the occasional serious one, the kids without obvious serious problems don’t have depressed IQ.
study  genetics  iq  QTL  🌞  survey  equilibrium  evolution  biodet  missing-heritability  nibble  roots  big-picture  s:*  behavioral-gen  chart  state-of-art  multi  west-hunter  sapiens  summary  neuro  intelligence  commentary  robust  paternal-age  sensitivity  perturbation  epidemiology  stylized-facts  scitariat  rot 
december 2016 by nhaliday
The Evolutionary Genetics of Personality Revisited
While mutations clearly affect the very low end of the intelligence continuum, individual differences in the normal intelligence range seem to be surprisingly robust against mutations, suggesting that they might have been canalized to withstand such perturbations. Most personality traits, by contrast, seem to be neither neutral to selection nor under consistent directional or stabilizing selection. Instead evidence is in line with balancing selection acting on personality traits, likely supported by human tendencies to seek out, construct and adapt to fitting environments.

shorter copy: http://www.larspenke.eu/pdfs/Penke_&_Jokela_2016_-_Evolutionary_Genetics_of_Personality_Revisited.pdf

The Evolutionary Genetics of Personality: http://www.larspenke.eu/pdfs/Penke_et_al_2007_-_Evolutionary_genetics_of_personality_target.pdf
Based on evolutionary genetic theory and empirical results from behaviour genetics and personality psychology, we conclude that selective neutrality is largely irrelevant, that mutation-selection balance seems best at explaining genetic variance in intelligence, and that balancing selection by environmental heterogeneity seems best at explaining genetic variance in personality traits. We propose a general model of heritable personality differences that conceptualises intelligence as fitness components and personality traits as individual reaction norms of genotypes across environments, with different fitness consequences in different environmental niches. We also discuss the place of mental health in the model.
study  spearhead  models  genetics  iq  personality  🌞  evopsych  evolution  sapiens  eden  pdf  explanation  survey  population-genetics  red-queen  metabuch  multi  EEA  essay  equilibrium  robust  big-picture  biodet  unit  QTL  len:long  sensitivity  perturbation  roots  EGT  deep-materialism  s:*  behavioral-gen  chart  intelligence  article  speculation  psychology  cog-psych  state-of-art 
december 2016 by nhaliday
What’s the catch? | West Hunter
Neanderthals and the Wrath of Khan

if someone were to try to create a Neanderthal a few years from now, starting with ancient DNA, they’d have to have worry a lot about data errors, because such errors would translate into mutations, which might be harmful or even lethal. Assume that we have figured out how to get the gene expression right, have all the proper methylation etc: we have modern humans as a template and you know there isn’t that much difference.

They might try consensus averaging – take three high-quality Neanderthal genomes and make your synthetic genome by majority rule: we ignore a nucleotide change in one genome if it’s not there in the other two. ‘tell me three times’, a simple form of error-correcting code.

But doing this would cause a problem. Can you see what the problem is?
west-hunter  sapiens  speculation  enhancement  archaics  discussion  genetics  genetic-load  🌞  gedanken  unintended-consequences  cocktail  error  aDNA  signal-noise  coding-theory  scitariat  wild-ideas  ideas  archaeology  perturbation  iteration-recursion  duplication  forms-instances  traces 
november 2016 by nhaliday

bundles : abstractphysics

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