nhaliday + gwas   121

Comparing within- and between-family polygenic score prediction | bioRxiv
https://twitter.com/StuartJRitchie/status/1116074740475736066
https://archive.is/bQnjM
See this thread for our new study on polygenic scores within fraternal twin pairs! Main point: take extra care with polygenic scores for traits like IQ & education, because they're confounded by (what seem to be) socioeconomic status effects. Not so for traits like height & BMI.
The idea is that the parenting is caused by the parental genotype, so it gets (mis)classified as a genetic effect on the children. It's really another way of looking at "genetic nurture" - see the papers from last year.
study  bio  preprint  biodet  behavioral-gen  genetics  sib-study  GWAS  class  s-factor  iq  education  attention  disease  psychiatry  embodied  health  environmental-effects  parenting  regularizer  spearhead  multi  twitter  social  commentary  backup 
10 days ago by nhaliday
Estimation of effect size distribution from genome-wide association studies and implications for future discoveries
We report a set of tools to estimate the number of susceptibility loci and the distribution of their effect sizes for a trait on the basis of discoveries from existing genome-wide association studies (GWASs). We propose statistical power calculations for future GWASs using estimated distributions of effect sizes. Using reported GWAS findings for height, Crohn’s disease and breast, prostate and colorectal (BPC) cancers, we determine that each of these traits is likely to harbor additional loci within the spectrum of low-penetrance common variants. These loci, which can be identified from sufficiently powerful GWASs, together could explain at least 15–20% of the known heritability of these traits. However, for BPC cancers, which have modest familial aggregation, our analysis suggests that risk models based on common variants alone will have modest discriminatory power (63.5% area under curve), even with new discoveries.

later paper:
Distribution of allele frequencies and effect sizes and their interrelationships for common genetic susceptibility variants: http://www.pnas.org/content/108/44/18026.full

Recent discoveries of hundreds of common susceptibility SNPs from genome-wide association studies provide a unique opportunity to examine population genetic models for complex traits. In this report, we investigate distributions of various population genetic parameters and their interrelationships using estimates of allele frequencies and effect-size parameters for about 400 susceptibility SNPs across a spectrum of qualitative and quantitative traits. We calibrate our analysis by statistical power for detection of SNPs to account for overrepresentation of variants with larger effect sizes in currently known SNPs that are expected due to statistical power for discovery. Across all qualitative disease traits, minor alleles conferred “risk” more often than “protection.” Across all traits, an inverse relationship existed between “regression effects” and allele frequencies. Both of these trends were remarkably strong for type I diabetes, a trait that is most likely to be influenced by selection, but were modest for other traits such as human height or late-onset diseases such as type II diabetes and cancers. Across all traits, the estimated effect-size distribution suggested the existence of increasingly large numbers of susceptibility SNPs with decreasingly small effects. For most traits, the set of SNPs with intermediate minor allele frequencies (5–20%) contained an unusually small number of susceptibility loci and explained a relatively small fraction of heritability compared with what would be expected from the distribution of SNPs in the general population. These trends could have several implications for future studies of common and uncommon variants.

...

Relationship Between Allele Frequency and Effect Size. We explored the relationship between allele frequency and effect size in different scales. An inverse relationship between the squared regression coefficient and f(1 − f) was observed consistently across different traits (Fig. 3). For a number of these traits, however, the strengths of these relationships become less pronounced after adjustment for ascertainment due to study power. The strength of the trend, as captured by the slope of the fitted line (Table 2), markedly varies between traits, with an almost 10-fold change between the two extremes of distinct types of traits. After adjustment, the most pronounced trend was seen for type I diabetes and Crohn’s disease among qualitative traits and LDL level among quantitative traits. In exploring the relationship between the frequency of the risk allele and the magnitude of the associated risk coefficient (Fig. S4), we observed a quadratic pattern that indicates increasing risk coefficients as the risk-allele frequency diverges away from 0.50 either toward 0 or toward 1. Thus, it appears that regression coefficients for common susceptibility SNPs increase in magnitude monotonically with decreasing minor-allele frequency, irrespective of whether the minor allele confers risk or protection. However, for some traits, such as type I diabetes, risk alleles were predominantly minor alleles, that is, they had frequencies of less than 0.50.
pdf  nibble  study  article  org:nat  🌞  biodet  genetics  population-genetics  GWAS  QTL  distribution  disease  cancer  stat-power  bioinformatics  magnitude  embodied  prediction  scale  scaling-up  variance-components  multi  missing-heritability  effect-size  regression  correlation  data 
november 2017 by nhaliday
Use and Interpretation of LD Score Regression
LD Score regression distinguishes confounding from polygenicity in genome-wide association studies: https://sci-hub.bz/10.1038/ng.3211
- Po-Ru Loh, Nick Patterson, et al.

https://www.biorxiv.org/content/biorxiv/early/2014/02/21/002931.full.pdf

Both polygenicity (i.e. many small genetic effects) and confounding biases, such as cryptic relatedness and population stratification, can yield inflated distributions of test statistics in genome-wide association studies (GWAS). However, current methods cannot distinguish between inflation from bias and true signal from polygenicity. We have developed an approach that quantifies the contributions of each by examining the relationship between test statistics and linkage disequilibrium (LD). We term this approach LD Score regression. LD Score regression provides an upper bound on the contribution of confounding bias to the observed inflation in test statistics and can be used to estimate a more powerful correction factor than genomic control. We find strong evidence that polygenicity accounts for the majority of test statistic inflation in many GWAS of large sample size.

Supplementary Note: https://images.nature.com/original/nature-assets/ng/journal/v47/n3/extref/ng.3211-S1.pdf

An atlas of genetic correlations across human diseases
and traits: https://sci-hub.bz/10.1038/ng.3406

https://www.biorxiv.org/content/early/2015/01/27/014498.full.pdf

Supplementary Note: https://images.nature.com/original/nature-assets/ng/journal/v47/n11/extref/ng.3406-S1.pdf

https://github.com/bulik/ldsc
ldsc is a command line tool for estimating heritability and genetic correlation from GWAS summary statistics. ldsc also computes LD Scores.
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november 2017 by nhaliday
Genome-wide association analysis identifies 30 new susceptibility loci for schizophrenia | Nature Genetics
We conducted a genome-wide association study (GWAS) with replication in 36,180 Chinese individuals and performed further transancestry meta-analyses with data from the Psychiatry Genomics Consortium (PGC2). Approximately 95% of the genome-wide significant (GWS) index alleles (or their proxies) from the PGC2 study were overrepresented in Chinese schizophrenia cases, including ∼50% that achieved nominal significance and ∼75% that continued to be GWS in the transancestry analysis. The Chinese-only analysis identified seven GWS loci; three of these also were GWS in the transancestry analyses, which identified 109 GWS loci, thus yielding a total of 113 GWS loci (30 novel) in at least one of these analyses. We observed improvements in the fine-mapping resolution at many susceptibility loci. Our results provide several lines of evidence supporting candidate genes at many loci and highlight some pathways for further research. Together, our findings provide novel insight into the genetic architecture and biological etiology of schizophrenia.
study  biodet  behavioral-gen  psychiatry  disease  GWAS  china  asia  race  generalization  genetics  replication 
november 2017 by nhaliday
Biopolitics | West Hunter
I have said before that no currently popular ideology acknowledges well-established results of behavioral genetics, quantitative genetics, or psychometrics. Or evolutionary psychology.

What if some ideology or political tradition did? what could they do? What problems could they solve, what capabilities would they have?

Various past societies knew a few things along these lines. They knew that there were significant physical and behavioral differences between the sexes, which is forbidden knowledge in modern academia. Some knew that close inbreeding had negative consequences, which knowledge is on its way to the forbidden zone as I speak. Some cultures with wide enough geographical experience had realistic notions of average cognitive differences between populations. Some people had a rough idea about regression to the mean [ in dynasties], and the Ottomans came up with a highly unpleasant solution – the law of fratricide. The Romans, during the Principate, dealt with the same problem through imperial adoption. The Chinese exam system is in part aimed at the same problem.

...

At least some past societies avoided the social patterns leading to the nasty dysgenic trends we are experiencing today, but for the most part that is due to the anthropic principle: if they’d done something else you wouldn’t be reading this. Also to between-group competition: if you fuck your self up when others don’t, you may be well be replaced. Which is still the case.

If you were designing an ideology from scratch you could make use of all of these facts – not that thinking about genetics and selection hands you the solution to every problem, but you’d have more strings to your bow. And, off the top of your head, you’d understand certain trends that are behind the mountains of Estcarp, for our current ruling classes : invisible and unthinkable, That Which Must Not Be Named. .

https://westhunt.wordpress.com/2017/10/08/biopolitics/#comment-96613
“The closest…s the sort of libertarianism promulgated by Charles Murray”
Not very close..
A government that was fully aware of the implications and possibilities of human genetics, one that had the usual kind of state goals [ like persistence and increased power] , would not necessarily be particularly libertarian.

https://westhunt.wordpress.com/2017/10/08/biopolitics/#comment-96797
And giving tax breaks to college-educated liberals to have babies wouldn’t appeal much to Trump voters, methinks.

It might be worth making a reasonably comprehensive of the facts and preferences that a good liberal is supposed to embrace and seem to believe. You would have to be fairly quick about it, before it changes. Then you could evaluate about the social impact of having more of them.

Rise and Fall: https://westhunt.wordpress.com/2018/01/18/rise-and-fall/
Every society selects for something: generally it looks as if the direction of selection pressue is more or less an accident. Although nations and empires in the past could have decided to select men for bravery or intelligence, there’s not much sign that anyone actually did this. I mean, they would have known how, if they’d wanted to, just as they knew how to select for destriers, coursers, and palfreys. It was still possible to know such things in the Middle Ages, because Harvard did not yet exist.

A rising empire needs quality human capital, which implies that at minimum that budding imperial society must not have been strongly dysgenic. At least not in the beginning. But winning changes many things, possibly including selective pressures. Imagine an empire with substantial urbanization, one in which talented guys routinely end up living in cities – cities that were demographic sinks. That might change things. Or try to imagine an empire in which survival challenges are greatly reduced, at least for elites, so that people have nothing to keep their minds off their minds and up worshiping Magna Mater. Imagine that an empire that conquers a rival with interesting local pathogens and brings some of them home. Or one that uses up a lot of its manpower conquering less-talented subjects and importing masses of those losers into the imperial heartland.

If any of those scenarios happened valid, they might eventually result in imperial decline – decline due to decreased biological capital.

Right now this is speculation. If we knew enough about the GWAS hits for intelligence, and had enough ancient DNA, we might be able to observe that rise and fall, just as we see dysgenic trends in contemporary populations. But that won’t happen for a long time. Say, a year.

hmm: https://westhunt.wordpress.com/2018/01/18/rise-and-fall/#comment-100350
“Although nations and empires in the past could have decided to select men for bravery or intelligence, there’s not much sign that anyone actually did this.”

Maybe the Chinese imperial examination could effectively have been a selection for intelligence.
--
Nope. I’ve modelled it: the fraction of winners is far too small to have much effect, while there were likely fitness costs from the arduous preparation. Moreover, there’s a recent
paper [Detecting polygenic adaptation in admixture graphs] that looks for indications of when selection for IQ hit northeast Asia: quite a while ago. Obvious though, since Japan has similar scores without ever having had that kind of examination system.

decline of British Empire and utility of different components: https://westhunt.wordpress.com/2018/01/18/rise-and-fall/#comment-100390
Once upon a time, India was a money maker for the British, mainly because they appropriate Bengali tax revenue, rather than trade. The rest of the Empire was not worth much: it didn’t materially boost British per-capita income or military potential. Silesia was worth more to Germany, conferred more war-making power, than Africa was to Britain.
--
If you get even a little local opposition, a colony won’t pay for itself. I seem to remember that there was some, in Palestine.
--
Angels from on high paid for the Boer War.

You know, someone in the 50’s asked for the numbers – how much various colonies cost and how much they paid.

Turned out that no one had ever asked. The Colonial Office had no idea.
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october 2017 by nhaliday
Accurate Genomic Prediction Of Human Height | bioRxiv
Stephen Hsu's compressed sensing application paper

We construct genomic predictors for heritable and extremely complex human quantitative traits (height, heel bone density, and educational attainment) using modern methods in high dimensional statistics (i.e., machine learning). Replication tests show that these predictors capture, respectively, ~40, 20, and 9 percent of total variance for the three traits. For example, predicted heights correlate ~0.65 with actual height; actual heights of most individuals in validation samples are within a few cm of the prediction.

https://infoproc.blogspot.com/2017/09/accurate-genomic-prediction-of-human.html

http://infoproc.blogspot.com/2017/11/23andme.html
I'm in Mountain View to give a talk at 23andMe. Their latest funding round was $250M on a (reported) valuation of $1.5B. If I just add up the Crunchbase numbers it looks like almost half a billion invested at this point...

Slides: Genomic Prediction of Complex Traits

Here's how people + robots handle your spit sample to produce a SNP genotype:

https://drive.google.com/file/d/1e_zuIPJr1hgQupYAxkcbgEVxmrDHAYRj/view
study  bio  preprint  GWAS  state-of-art  embodied  genetics  genomics  compressed-sensing  high-dimension  machine-learning  missing-heritability  hsu  scitariat  education  🌞  frontier  britain  regression  data  visualization  correlation  phase-transition  multi  commentary  summary  pdf  slides  brands  skunkworks  hard-tech  presentation  talks  methodology  intricacy  bioinformatics  scaling-up  stat-power  sparsity  norms  nibble  speedometer  stats  linear-models  2017  biodet 
september 2017 by nhaliday
The Genetics of Alzheimer Disease
Twin and family studies indicate that genetic factors are estimated to play a role in at least 80% of AD cases. The inheritance of AD exhibits a dichotomous pattern. On one hand, rare mutations in APP, PSEN1, and PSEN2 virtually guarantee early-onset (<60 years) familial AD, which represents ∼5% of AD. On the other hand, common gene polymorphisms, such as the ε4 and ε2 variants of the APOE gene, can influence susceptibility for ∼50% of the common late-onset AD. These four genes account for 30%–50% of the inheritability of AD. Genome-wide association studies have recently led to the identification of 11 additional AD candidate genes.

Role of Genes and Environments for Explaining Alzheimer Disease: http://jamanetwork.com/journals/jamapsychiatry/fullarticle/209307
study  biodet  twin-study  sib-study  variance-components  candidate-gene  GWAS  medicine  neuro  neuro-nitgrit  dementia  disease  🌞  aging  multi  org:nat  genetics  genomics  immune  health 
september 2017 by nhaliday
trees are harlequins, words are harlequins — bayes: a kinda-sorta masterpost
lol, gwern: https://www.reddit.com/r/slatestarcodex/comments/6ghsxf/biweekly_rational_feed/diqr0rq/
> What sort of person thinks “oh yeah, my beliefs about these coefficients correspond to a Gaussian with variance 2.5″? And what if I do cross-validation, like I always do, and find that variance 200 works better for the problem? Was the other person wrong? But how could they have known?
> ...Even ignoring the mode vs. mean issue, I have never met anyone who could tell whether their beliefs were normally distributed vs. Laplace distributed. Have you?
I must have spent too much time in Bayesland because both those strike me as very easy and I often think them! My beliefs usually are Laplace distributed when it comes to things like genetics (it makes me very sad to see GWASes with flat priors), and my Gaussian coefficients are actually a variance of 0.70 (assuming standardized variables w.l.o.g.) as is consistent with field-wide meta-analyses indicating that d>1 is pretty rare.
ratty  ssc  core-rats  tumblr  social  explanation  init  philosophy  bayesian  thinking  probability  stats  frequentist  big-yud  lesswrong  synchrony  similarity  critique  intricacy  shalizi  scitariat  selection  mutation  evolution  priors-posteriors  regularization  bias-variance  gwern  reddit  commentary  GWAS  genetics  regression  spock  nitty-gritty  generalization  epistemic  🤖  rationality  poast  multi  best-practices  methodology  data-science 
august 2017 by nhaliday
Polygenic Adaptation has Impacted Multiple Anthropometric Traits | bioRxiv
By comparing these polygenic scores to a null distribution under genetic drift, we identify strong signals of selection for a suite of anthropometric traits including height, infant head circumference (IHC), hip circumference (HIP) and waist-to-hip ratio (WHR), as well as type 2 diabetes (T2D). In addition to the known north-south gradient of polygenic height scores within Europe, we find that natural selection has contributed to a gradient of decreasing polygenic height scores from West to East across Eurasia, and that this gradient is consistent with selection on height in ancient populations who have contributed ancestry broadly across Eurasia. We find that the signal of selection on HIP can largely be explained as a correlated response to selection on height. However, our signals in IHC and WC/WHR cannot, suggesting a response to selection along multiple axes of body shape variation. Our observation that IHC, WC, and WHR polygenic scores follow a strong latitudinal cline in Western Eurasia support the role of natural selection in establishing Bergmann's Rule in humans, and are consistent with thermoregulatory adaptation in response to latitudinal temperature variation.

http://infoproc.blogspot.com/2017/07/natural-selection-and-body-shape-in.html
study  bio  preprint  biodet  genetics  evolution  sapiens  pop-diff  embodied  recent-selection  survey  🌞  europe  asia  shift  GWAS  population-genetics  pop-structure  spearhead  environment  temperature  correlation  multi  hsu  scitariat  commentary 
july 2017 by nhaliday
A combined analysis of genetically correlated traits identifies 107 loci associated with intelligence | bioRxiv
We apply MTAG to three large GWAS: Sniekers et al (2017) on intelligence, Okbay et al. (2016) on Educational attainment, and Hill et al. (2016) on household income. By combining these three samples our functional sample size increased from 78 308 participants to 147 194. We found 107 independent loci associated with intelligence, implicating 233 genes, using both SNP-based and gene-based GWAS. We find evidence that neurogenesis may explain some of the biological differences in intelligence as well as genes expressed in the synapse and those involved in the regulation of the nervous system.

...

Finally, using an independent sample of 6 844 individuals we were able to predict 7% of intelligence using SNP data alone.
study  bio  preprint  biodet  behavioral-gen  GWAS  genetics  iq  education  compensation  composition-decomposition  🌞  gwern  meta-analysis  genetic-correlation  scaling-up  methodology  correlation  state-of-art  neuro  neuro-nitgrit  dimensionality 
july 2017 by nhaliday
Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders : Nature Genetics : Nature Research
Autism spectrum disorder (ASD) risk is influenced by common polygenic and de novo variation. We aimed to clarify the influence of polygenic risk for ASD and to identify subgroups of ASD cases, including those with strongly acting de novo variants, in which polygenic risk is relevant. Using a novel approach called the polygenic transmission disequilibrium test and data from 6,454 families with a child with ASD, we show that polygenic risk for ASD, schizophrenia, and greater educational attainment is over-transmitted to children with ASD. These findings hold independent of proband IQ. We find that polygenic variation contributes additively to risk in ASD cases who carry a strongly acting de novo variant. Lastly, we show that elements of polygenic risk are independent and differ in their relationship with phenotype. These results confirm that the genetic influences on ASD are additive and suggest that they create risk through at least partially distinct etiologic pathways.

https://en.wikipedia.org/wiki/Transmission_disequilibrium_test
study  biodet  behavioral-gen  genetics  population-genetics  QTL  missing-heritability  psychiatry  autism  👽  disease  org:nat  🌞  gwern  pdf  piracy  education  multi  methodology  wiki  reference  psychology  cog-psych  genetic-load  genetic-correlation  sib-study  hypothesis-testing  equilibrium  iq  correlation  intricacy  GWAS  causation  endo-exo  endogenous-exogenous 
july 2017 by nhaliday
A genome-wide polygenic approach to HIV uncovers link to inflammatory bowel disease and identifies potential novel genetic variants | bioRxiv
We further showed that the genetic overlap between HIV acquisition and schizophrenia is likely driven in part by their shared overlap with cannabis use and sexual behavior.
study  bio  preprint  biodet  behavioral-gen  GWAS  genetic-correlation  correlation  trivia  cocktail  disease  sex  sexuality  drugs  psychiatry  genetics 
june 2017 by nhaliday
The Genomic Health Of Ancient Hominins | bioRxiv
On a broad scale, hereditary disease risks are similar for ancient hominins and modern-day humans, and the GRS percentiles of ancient individuals span the full range of what is observed in present day individuals. In addition, there is evidence that ancient pastoralists may have had healthier genomes than hunter-gatherers and agriculturalists. We also observed a temporal trend whereby genomes from the recent past are more likely to be healthier than genomes from the deep past.

Gwern has interesting take (abstract is misleading): https://twitter.com/gwern/status/871061144152178688

here it is in conclusion (and cf Figure 3A):
The genomic health of ancient individuals appears to have improved over time (Figure 3B). This calls into question the idea that genetic load has been increasing in human populations (Lynch 2016). However, there exists a perplexing pattern: ancient individuals who lived within the last few thousand years have healthier genomes, on average, than present day humans.

http://www.pnas.org/content/early/2017/08/08/1703856114
After controlling for age, BMI, and other variables, knee OA prevalence was 2.1-fold higher (95% confidence interval, 1.5–3.1) in the postindustrial sample than in the early industrial sample. Our results indicate that increases in longevity and BMI are insufficient to explain the approximate doubling of knee OA prevalence that has occurred in the United States since the mid-20th century. Knee OA is thus more preventable than is commonly assumed, but prevention will require research on additional independent risk factors that either arose or have become amplified in the postindustrial era.
study  bio  preprint  sapiens  genetics  biodet  disease  health  history  antiquity  aDNA  farmers-and-foragers  agriculture  anthropology  GWAS  genetic-load  multi  twitter  social  commentary  gwern  dysgenics  trends  mutation  embodied  org:nat  obesity  public-health  epidemiology  🌞  science-anxiety 
june 2017 by nhaliday
Genomic analysis of family data reveals additional genetic effects on intelligence and personality | bioRxiv
methodology:
Using Extended Genealogy to Estimate Components of Heritability for 23 Quantitative and Dichotomous Traits: http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1003520
Pedigree- and SNP-Associated Genetics and Recent Environment are the Major Contributors to Anthropometric and Cardiometabolic Trait Variation: http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005804

Missing Heritability – found?: https://westhunt.wordpress.com/2017/02/09/missing-heritability-found/
There is an interesting new paper out on genetics and IQ. The claim is that they have found the missing heritability – in rare variants, generally different in each family.

Some of the variants, the ones we find with GWAS, are fairly common and fitness-neutral: the variant that slightly increases IQ confers the same fitness (or very close to the same) as the one that slightly decreases IQ – presumably because of other effects it has. If this weren’t the case, it would be impossible for both of the variants to remain common.

The rare variants that affect IQ will generally decrease IQ – and since pleiotropy is the norm, usually they’ll be deleterious in other ways as well. Genetic load.

Happy families are all alike; every unhappy family is unhappy in its own way.: https://westhunt.wordpress.com/2017/06/06/happy-families-are-all-alike-every-unhappy-family-is-unhappy-in-its-own-way/
It now looks as if the majority of the genetic variance in IQ is the product of mutational load, and the same may be true for many psychological traits. To the extent this is the case, a lot of human psychological variation must be non-adaptive. Maybe some personality variation fulfills an evolutionary function, but a lot does not. Being a dumb asshole may be a bug, rather than a feature. More generally, this kind of analysis could show us whether particular low-fitness syndromes, like autism, were ever strategies – I suspect not.

It’s bad new news for medicine and psychiatry, though. It would suggest that what we call a given type of mental illness, like schizophrenia, is really a grab-bag of many different syndromes. The ultimate causes are extremely varied: at best, there may be shared intermediate causal factors. Not good news for drug development: individualized medicine is a threat, not a promise.

see also comment at: https://pinboard.in/u:nhaliday/b:a6ab4034b0d0

https://www.reddit.com/r/slatestarcodex/comments/5sldfa/genomic_analysis_of_family_data_reveals/
So the big implication here is that it's better than I had dared hope - like Yang/Visscher/Hsu have argued, the old GCTA estimate of ~0.3 is indeed a rather loose lower bound on additive genetic variants, and the rest of the missing heritability is just the relatively uncommon additive variants (ie <1% frequency), and so, like Yang demonstrated with height, using much more comprehensive imputation of SNP scores or using whole-genomes will be able to explain almost all of the genetic contribution. In other words, with better imputation panels, we can go back and squeeze out better polygenic scores from old GWASes, new GWASes will be able to reach and break the 0.3 upper bound, and eventually we can feasibly predict 0.5-0.8. Between the expanding sample sizes from biobanks, the still-falling price of whole genomes, the gradual development of better regression methods (informative priors, biological annotation information, networks, genetic correlations), and better imputation, the future of GWAS polygenic scores is bright. Which obviously will be extremely helpful for embryo selection/genome synthesis.

The argument that this supports mutation-selection balance is weaker but plausible. I hope that it's true, because if that's why there is so much genetic variation in intelligence, then that strongly encourages genetic engineering - there is no good reason or Chesterton fence for intelligence variants being non-fixed, it's just that evolution is too slow to purge the constantly-accumulating bad variants. And we can do better.
https://rubenarslan.github.io/generation_scotland_pedigree_gcta/

The surprising implications of familial association in disease risk: https://arxiv.org/abs/1707.00014
https://spottedtoad.wordpress.com/2017/06/09/personalized-medicine-wont-work-but-race-based-medicine-probably-will/
As Greg Cochran has pointed out, this probably isn’t going to work. There are a few genes like BRCA1 (which makes you more likely to get breast and ovarian cancer) that we can detect and might affect treatment, but an awful lot of disease turns out to be just the result of random chance and deleterious mutation. This means that you can’t easily tailor disease treatment to people’s genes, because everybody is fucked up in their own special way. If Johnny is schizophrenic because of 100 random errors in the genes that code for his neurons, and Jack is schizophrenic because of 100 other random errors, there’s very little way to test a drug to work for either of them- they’re the only one in the world, most likely, with that specific pattern of errors. This is, presumably why the incidence of schizophrenia and autism rises in populations when dads get older- more random errors in sperm formation mean more random errors in the baby’s genes, and more things that go wrong down the line.

The looming crisis in human genetics: http://www.economist.com/node/14742737
Some awkward news ahead
- Geoffrey Miller

Human geneticists have reached a private crisis of conscience, and it will become public knowledge in 2010. The crisis has depressing health implications and alarming political ones. In a nutshell: the new genetics will reveal much less than hoped about how to cure disease, and much more than feared about human evolution and inequality, including genetic differences between classes, ethnicities and races.

2009!
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june 2017 by nhaliday
Edge.org: 2017 : WHAT SCIENTIFIC TERM OR CONCEPT OUGHT TO BE MORE WIDELY KNOWN?
highlights:
- the genetic book of the dead [Dawkins]
- complementarity [Frank Wilczek]
- relative information
- effective theory [Lisa Randall]
- affordances [Dennett]
- spontaneous symmetry breaking
- relatedly, equipoise [Nicholas Christakis]
- case-based reasoning
- population reasoning (eg, common law)
- criticality [Cesar Hidalgo]
- Haldan's law of the right size (!SCALE!)
- polygenic scores
- non-ergodic
- ansatz
- state [Aaronson]: http://www.scottaaronson.com/blog/?p=3075
- transfer learning
- effect size
- satisficing
- scaling
- the breeder's equation [Greg Cochran]
- impedance matching

soft:
- reciprocal altruism
- life history [Plomin]
- intellectual honesty [Sam Harris]
- coalitional instinct (interesting claim: building coalitions around "rationality" actually makes it more difficult to update on new evidence as it makes you look like a bad person, eg, the Cathedral)
basically same: https://twitter.com/ortoiseortoise/status/903682354367143936

more: https://www.edge.org/conversation/john_tooby-coalitional-instincts

interesting timing. how woke is this dude?
org:edge  2017  technology  discussion  trends  list  expert  science  top-n  frontier  multi  big-picture  links  the-world-is-just-atoms  metameta  🔬  scitariat  conceptual-vocab  coalitions  q-n-a  psychology  social-psych  anthropology  instinct  coordination  duty  power  status  info-dynamics  cultural-dynamics  being-right  realness  cooperate-defect  westminster  chart  zeitgeist  rot  roots  epistemic  rationality  meta:science  analogy  physics  electromag  geoengineering  environment  atmosphere  climate-change  waves  information-theory  bits  marginal  quantum  metabuch  homo-hetero  thinking  sapiens  genetics  genomics  evolution  bio  GT-101  low-hanging  minimum-viable  dennett  philosophy  cog-psych  neurons  symmetry  humility  life-history  social-structure  GWAS  behavioral-gen  biodet  missing-heritability  ergodic  machine-learning  generalization  west-hunter  population-genetics  methodology  blowhards  spearhead  group-level  scale  magnitude  business  scaling-tech  tech  business-models  optimization  effect-size  aaronson  state  bare-hands  problem-solving  politics 
may 2017 by nhaliday
Missing heritability problem - Wikipedia
The "missing heritability" problem[1][2][3][4][5][6] can be defined as the fact that single genetic variations cannot account for much of the heritability of diseases, behaviors, and other phenotypes. This is a problem that has significant implications for medicine, since a person's susceptibility to disease may depend more on "the combined effect of all the genes in the background than on the disease genes in the foreground", or the role of genes may have been severely overestimated.

The 'missing heritability' problem was named as such in 2008. The Human Genome Project led to optimistic forecasts that the large genetic contributions to many traits and diseases (which were identified by quantitative genetics and behavioral genetics in particular) would soon be mapped and pinned down to specific genes and their genetic variants by methods such as candidate-gene studies which used small samples with limited genetic sequencing to focus on specific genes believed to be involved, examining the SNP kinds of variants. While many hits were found, they often failed to replicate in other studies.

The exponential fall in genome sequencing costs led to the use of GWAS studies which could simultaneously examine all candidate-genes in larger samples than the original finding, where the candidate-gene hits were found to almost always be false positives and only 2-6% replicate;[7][8][9][10][11][12] in the specific case of intelligence candidate-gene hits, only 1 candidate-gene hit replicated,[13] and of 15 neuroimaging hits, none did.[14] The editorial board of Behavior Genetics noted, in setting more stringent requirements for candidate-gene publications, that "the literature on candidate gene associations is full of reports that have not stood up to rigorous replication...it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge".[15] Other researchers have characterized the literature as having "yielded an infinitude of publications with very few consistent replications" and called for a phase out of candidate-gene studies in favor of polygenic scores.[16]

This led to a dilemma. Standard genetics methods have long estimated large heritabilities such as 80% for traits such as height or intelligence, yet none of the genes had been found despite sample sizes that, while small, should have been able to detect variants of reasonable effect size such as 1 inch or 5 IQ points. If genes have such strong cumulative effects - where were they? Several resolutions have been proposed, that the missing heritability is some combination of:

...

7. Genetic effects are indeed through common SNPs acting additively, but are highly polygenic: dispersed over hundreds or thousands of variants each of small effect like a fraction of an inch or a fifth of an IQ point and with low prior probability: unexpected enough that a candidate-gene study is unlikely to select the right SNP out of hundreds of thousands of known SNPs, and GWASes up to 2010, with n<20000, would be unable to find hits which reach genome-wide statistical-significance thresholds. Much larger GWAS sample sizes, often n>100k, would be required to find any hits at all, and would steadily increase after that.
This resolution to the missing heritability problem was supported by the introduction of Genome-wide complex trait analysis (GCTA) in 2010, which demonstrated that trait similarity could be predicted by the genetic similarity of unrelated strangers on common SNPs treated additively, and for many traits the SNP heritability was indeed a substantial fraction of the overall heritability. The GCTA results were further buttressed by findings that a small percent of trait variance could be predicted in GWASes without any genome-wide statistically-significant hits by a linear model including all SNPs regardless of p-value; if there were no SNP contribution, this would be unlikely, but it would be what one expected from SNPs whose effects were very imprecisely estimated by a too-small sample. Combined with the upper bound on maximum effect sizes set by the GWASes up to then, this strongly implied that the highly polygenic theory was correct. Examples of complex traits where increasingly large-scale GWASes have yielded the initial hits and then increasing numbers of hits as sample sizes increased from n<20k to n>100k or n>300k include height,[23] intelligence,[24] and schizophrenia.
article  bio  biodet  behavioral-gen  genetics  genomics  GWAS  candidate-gene  methodology  QTL  missing-heritability  twin-study  measurement  epigenetics  nonlinearity  error  history  mostly-modern  reflection  wiki  reference  science  bounded-cognition  replication  being-right  info-dynamics  🌞  linearity  ideas  GCTA  spearhead 
may 2017 by nhaliday
Intersection of diverse neuronal genomes and neuropsychiatric disease: The Brain Somatic Mosaicism Network
Towards explaining non-shared-environment effects on intelligence, psychiatric disorders, and other cognitive traits - developmental noise such as post-conception mutations in individual cells or groups of cells
pdf  study  psychology  cog-psych  neuro  neuro-nitgrit  brain-scan  biodet  genetics  genomics  GWAS  🌞  psychiatry  behavioral-gen  mutation  environmental-effects  roots  org:nat  gwern  random  autism  proposal  signal-noise  developmental  composition-decomposition 
may 2017 by nhaliday
Soft sweeps are the dominant mode of adaptation in the human genome | bioRxiv
Detection of 2000 instances of recent human selection, half of which are specific to individual human populations, and many of which affect the central nervous system. Note this doesn’t cover polygenic selection, so it’s a very loose lower bound on how much recent human evolution there has been.

How Sweeps Get Soft: https://westhunt.wordpress.com/2011/09/29/how-sweeps-get-soft/
A puzzling finding from the search for selection in humans is the large number of apparently selected variants versus the apparent absence of high frequency selected regions and regions that have become fixed in our species.

Cochran, John Hawks, and I were involved in some of this work, and we all thought immediately without any discussion that the intermediate frequency sweeps must reflect heterozygote advantage.
study  preprint  bio  sapiens  recent-selection  genetics  selection  stylized-facts  evolution  genomics  GWAS  🌞  population-genetics  gwern  methodology  multi  west-hunter  explanation  gene-flow  scitariat  hetero-advantage  genetic-load  pop-structure  race  europe  africa  migration  gene-drift 
may 2017 by nhaliday
Secular decline in testosterone levels - Rogue Health and Fitness
A Population-Level Decline in Serum Testosterone Levels in American Men: http://sci-hub.tw/10.1210/jc.2006-1375
Secular trends in sex hormones and fractures in men and women: http://www.eje-online.org/content/166/5/887.full.pdf
https://twitter.com/toad_spotted/status/984543033285898246
https://archive.is/dcruu
Small n and older sample, but interesting that while testosterone decreases have been large for men they’ve been even larger (in % terms) for women; wonder if this contributes to declining pregnancy and sexual frequency, rising depression.

https://www.labcorp.com/assets/11476
http://www.theamericanconservative.com/articles/sperm-killers-and-rising-male-infertility/
https://www.theguardian.com/lifeandstyle/2017/jul/25/sperm-counts-among-western-men-have-halved-in-last-40-years-study
https://www.weforum.org/agenda/2017/08/most-men-in-the-us-and-europe-could-be-infertile-by-2060
Strangelove: https://youtu.be/N1KvgtEnABY?t=67

https://www.scientificamerican.com/article/sperm-count-dropping-in-western-world/
https://news.ycombinator.com/item?id=14855796
https://news.ycombinator.com/item?id=14857588
People offering human-centric explanations like cell phones: Note also that the sperm quality of dogs has decreased 30% since 1988.

mendelian rand.:
https://www.ncbi.nlm.nih.gov/pubmed/28448539
1 SD genetically instrumented increase in BMI was associated with a 0.25 SD decrease in serum testosterone
https://twitter.com/SilverVVulpes/status/857902555489341441

Ibuprofen linked to male infertility: study: https://nypost.com/2018/01/08/ibuprofen-linked-to-male-infertility-study/
http://www.pnas.org/content/115/4/E715.full

Tucker Carlson: "Men Seem To Be Becoming Less Male": https://www.realclearpolitics.com/video/2018/03/08/tucker_carlson_men_seem_to_be_becoming_less_male.html
Carlson interviewed Dr. Jordan Peterson who blamed the "insidious" movement being driven by the "radical left" that teaches there a problem of "toxic masculinity." He said ideological policies focus on "de-emphasizing masculinity may be part of the problem."

...

Those are the numbers. They paint a very clear picture: American men are failing, in body, mind and spirit. This is a crisis. Yet our leaders pretend it’s not happening. They tell us the opposite is true: Women are victims, men are oppressors. To question that assumption is to risk punishment. Even as women far outpace men in higher education, virtually every college campus supports a women’s studies department, whose core goal is to attack male power. Our politicians and business leaders internalize and amplify that message. Men are privileged. Women are oppressed. Hire and promote and reward accordingly.

https://pinboard.in/u:nhaliday/b:bd7b0a50d741
But it also hints at an almost opposite take: average testosterone levels have been falling for decades, so at this point these businessmen would be the only “normal” (by 1950s standards) men out there, and everyone else would be unprecedently risk-averse and boring.
org:health  fitsci  health  endocrine  trends  public-health  science-anxiety  gender  commentary  multi  study  pdf  data  piracy  white-paper  gnon  news  org:mag  right-wing  fertility  dysgenics  drugs  psychiatry  stress  politics  government  hypochondria  idk  embodied  FDA  externalities  epidemiology  video  film  classic  org:lite  org:anglo  genetics  endo-exo  mendel-randomization  obesity  fitness  scitariat  🌞  medicine  correlation  intervention  causation  GWAS  environmental-effects  hn  org:sci  popsci  model-organism  embodied-cognition  hmm  org:davos  communism  memes(ew)  fluid  endogenous-exogenous  roots  explanans  org:local  summary  modernity  rot  org:nat  chart  the-bones  albion  canada  journos-pundits  philosophy  iq  coming-apart  malaise  gender-diff  attention  disease  opioids  death  interview  current-events  tv  higher-ed  labor  management  compensation  grad-school  law  twitter  social  backup  ratty  unaffiliated  yvain  ssc 
may 2017 by nhaliday
The Ionian Mission | West Hunter
I have have had famous people ask me how the Ionian Greeks became so smart (in Classical times, natch). In Classical times, the Greeks – particularly the Ionian Greeks – gave everybody this impression – in everyday experience, and certainly in terms of production of outstanding intellects. Everybody thought so. Nobody said this about the Persians – and nobody said it about the Jews, who never said it about themselves.

It’s an interesting question: perhaps there was some process analogous to that which we have proposed as an explanation for the high intelligence of the Ashkenazi Jews. Or maybe something else happened – a different selective process, or maybe it was all cultural. It’s hard to know – the Greek Dark Ages, the long period of illiteracy after the fall of Mycenaean civilization, is poorly understood, certainly by me.

Suppose that your biological IQ capacity (in favorable conditions) is set by a few hundred or thousand SNPS, and that we have identified those SNPS. With luck, we might find enough skeletons with intact DNA to see if the Ionian Greeks really were smarter than the average bear, and how that changed over time.

More generally, we could see if civilization boosted or decreased IQ, in various situations. This could be a big part of the historical process – civilizations falling because average competence has dropped, science being born because the population is now ready for it…

I think we’ll be ready to try this in a year or two. The biggest problems will be political, since this approach would also predict results in existing populations – although that would probably not be very interesting, since we already know all those results.

The Ancient Greeks Weren’t All Geniuses: http://www.unz.com/akarlin/ancient-greeks-not-geniuses/
west-hunter  scitariat  history  iron-age  mediterranean  the-classics  iq  pop-diff  aDNA  civilization  leviathan  GWAS  genetics  biodet  behavioral-gen  anthropology  sapiens  speculation  discussion  recent-selection  archaeology  virtu  cycles  oscillation  broad-econ  microfoundations  multi  gnon  commentary  quotes  galton  giants  old-anglo  psychometrics  malthus  health  embodied  kinship  parasites-microbiome  china  asia  innovation  frontier  demographics  environmental-effects  alien-character  🌞  debate 
april 2017 by nhaliday
Educational Romanticism & Economic Development | pseudoerasmus
https://twitter.com/GarettJones/status/852339296358940672
deleeted

https://twitter.com/GarettJones/status/943238170312929280
https://archive.is/p5hRA

Did Nations that Boosted Education Grow Faster?: http://econlog.econlib.org/archives/2012/10/did_nations_tha.html
On average, no relationship. The trendline points down slightly, but for the time being let's just call it a draw. It's a well-known fact that countries that started the 1960's with high education levels grew faster (example), but this graph is about something different. This graph shows that countries that increased their education levels did not grow faster.

Where has all the education gone?: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.1016.2704&rep=rep1&type=pdf

https://twitter.com/GarettJones/status/948052794681966593
https://archive.is/kjxqp

https://twitter.com/GarettJones/status/950952412503822337
https://archive.is/3YPic

https://twitter.com/pseudoerasmus/status/862961420065001472
http://hanushek.stanford.edu/publications/schooling-educational-achievement-and-latin-american-growth-puzzle

The Case Against Education: What's Taking So Long, Bryan Caplan: http://econlog.econlib.org/archives/2015/03/the_case_agains_9.html

The World Might Be Better Off Without College for Everyone: https://www.theatlantic.com/magazine/archive/2018/01/whats-college-good-for/546590/
Students don't seem to be getting much out of higher education.
- Bryan Caplan

College: Capital or Signal?: http://www.economicmanblog.com/2017/02/25/college-capital-or-signal/
After his review of the literature, Caplan concludes that roughly 80% of the earnings effect from college comes from signalling, with only 20% the result of skill building. Put this together with his earlier observations about the private returns to college education, along with its exploding cost, and Caplan thinks that the social returns are negative. The policy implications of this will come as very bitter medicine for friends of Bernie Sanders.

Doubting the Null Hypothesis: http://www.arnoldkling.com/blog/doubting-the-null-hypothesis/

Is higher education/college in the US more about skill-building or about signaling?: https://www.quora.com/Is-higher-education-college-in-the-US-more-about-skill-building-or-about-signaling
ballpark: 50% signaling, 30% selection, 20% addition to human capital
more signaling in art history, more human capital in engineering, more selection in philosophy

Econ Duel! Is Education Signaling or Skill Building?: http://marginalrevolution.com/marginalrevolution/2016/03/econ-duel-is-education-signaling-or-skill-building.html
Marginal Revolution University has a brand new feature, Econ Duel! Our first Econ Duel features Tyler and me debating the question, Is education more about signaling or skill building?

Against Tulip Subsidies: https://slatestarcodex.com/2015/06/06/against-tulip-subsidies/

https://www.overcomingbias.com/2018/01/read-the-case-against-education.html

https://nintil.com/2018/02/05/notes-on-the-case-against-education/

https://www.nationalreview.com/magazine/2018-02-19-0000/bryan-caplan-case-against-education-review

https://spottedtoad.wordpress.com/2018/02/12/the-case-against-education/
Most American public school kids are low-income; about half are non-white; most are fairly low skilled academically. For most American kids, the majority of the waking hours they spend not engaged with electronic media are at school; the majority of their in-person relationships are at school; the most important relationships they have with an adult who is not their parent is with their teacher. For their parents, the most important in-person source of community is also their kids’ school. Young people need adult mirrors, models, mentors, and in an earlier era these might have been provided by extended families, but in our own era this all falls upon schools.

Caplan gestures towards work and earlier labor force participation as alternatives to school for many if not all kids. And I empathize: the years that I would point to as making me who I am were ones where I was working, not studying. But they were years spent working in schools, as a teacher or assistant. If schools did not exist, is there an alternative that we genuinely believe would arise to draw young people into the life of their community?

...

It is not an accident that the state that spends the least on education is Utah, where the LDS church can take up some of the slack for schools, while next door Wyoming spends almost the most of any state at $16,000 per student. Education is now the one surviving binding principle of the society as a whole, the one black box everyone will agree to, and so while you can press for less subsidization of education by government, and for privatization of costs, as Caplan does, there’s really nothing people can substitute for it. This is partially about signaling, sure, but it’s also because outside of schools and a few religious enclaves our society is but a darkling plain beset by winds.

This doesn’t mean that we should leave Caplan’s critique on the shelf. Much of education is focused on an insane, zero-sum race for finite rewards. Much of schooling does push kids, parents, schools, and school systems towards a solution ad absurdum, where anything less than 100 percent of kids headed to a doctorate and the big coding job in the sky is a sign of failure of everyone concerned.

But let’s approach this with an eye towards the limits of the possible and the reality of diminishing returns.

https://westhunt.wordpress.com/2018/01/27/poison-ivy-halls/
https://westhunt.wordpress.com/2018/01/27/poison-ivy-halls/#comment-101293
The real reason the left would support Moander: the usual reason. because he’s an enemy.

https://westhunt.wordpress.com/2018/02/01/bright-college-days-part-i/
I have a problem in thinking about education, since my preferences and personal educational experience are atypical, so I can’t just gut it out. On the other hand, knowing that puts me ahead of a lot of people that seem convinced that all real people, including all Arab cabdrivers, think and feel just as they do.

One important fact, relevant to this review. I don’t like Caplan. I think he doesn’t understand – can’t understand – human nature, and although that sometimes confers a different and interesting perspective, it’s not a royal road to truth. Nor would I want to share a foxhole with him: I don’t trust him. So if I say that I agree with some parts of this book, you should believe me.

...

Caplan doesn’t talk about possible ways of improving knowledge acquisition and retention. Maybe he thinks that’s impossible, and he may be right, at least within a conventional universe of possibilities. That’s a bit outside of his thesis, anyhow. Me it interests.

He dismisses objections from educational psychologists who claim that studying a subject improves you in subtle ways even after you forget all of it. I too find that hard to believe. On the other hand, it looks to me as if poorly-digested fragments of information picked up in college have some effect on public policy later in life: it is no coincidence that most prominent people in public life (at a given moment) share a lot of the same ideas. People are vaguely remembering the same crap from the same sources, or related sources. It’s correlated crap, which has a much stronger effect than random crap.

These widespread new ideas are usually wrong. They come from somewhere – in part, from higher education. Along this line, Caplan thinks that college has only a weak ideological effect on students. I don’t believe he is correct. In part, this is because most people use a shifting standard: what’s liberal or conservative gets redefined over time. At any given time a population is roughly half left and half right – but the content of those labels changes a lot. There’s a shift.

https://westhunt.wordpress.com/2018/02/01/bright-college-days-part-i/#comment-101492
I put it this way, a while ago: “When you think about it, falsehoods, stupid crap, make the best group identifiers, because anyone might agree with you when you’re obviously right. Signing up to clear nonsense is a better test of group loyalty. A true friend is with you when you’re wrong. Ideally, not just wrong, but barking mad, rolling around in your own vomit wrong.”
--
You just explained the Credo quia absurdum doctrine. I always wondered if it was nonsense. It is not.
--
Someone on twitter caught it first – got all the way to “sliding down the razor blade of life”. Which I explained is now called “transitioning”

What Catholics believe: https://theweek.com/articles/781925/what-catholics-believe
We believe all of these things, fantastical as they may sound, and we believe them for what we consider good reasons, well attested by history, consistent with the most exacting standards of logic. We will profess them in this place of wrath and tears until the extraordinary event referenced above, for which men and women have hoped and prayed for nearly 2,000 years, comes to pass.

https://westhunt.wordpress.com/2018/02/05/bright-college-days-part-ii/
According to Caplan, employers are looking for conformity, conscientiousness, and intelligence. They use completion of high school, or completion of college as a sign of conformity and conscientiousness. College certainly looks as if it’s mostly signaling, and it’s hugely expensive signaling, in terms of college costs and foregone earnings.

But inserting conformity into the merit function is tricky: things become important signals… because they’re important signals. Otherwise useful actions are contraindicated because they’re “not done”. For example, test scores convey useful information. They could help show that an applicant is smart even though he attended a mediocre school – the same role they play in college admissions. But employers seldom request test scores, and although applicants may provide them, few do. Caplan says ” The word on the street… [more]
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april 2017 by nhaliday
Genome-Wide Association Study Reveals Multiple Loci Influencing Normal Human Facial Morphology
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0099009
https://twitter.com/dgmacarthur/status/904908988516585472
https://twitter.com/piper_jason/status/905128320869662720
http://www.biorxiv.org/content/early/2017/09/07/185330
https://www.technologyreview.com/s/608813/does-your-genome-predict-your-face-not-quite-yet/

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000451
Domestic dogs exhibit tremendous phenotypic diversity, including a greater variation in body size than any other terrestrial mammal. Here, we generate a high density map of canine genetic variation by genotyping 915 dogs from 80 domestic dog breeds, 83 wild canids, and 10 outbred African shelter dogs across 60,968 single-nucleotide polymorphisms (SNPs). Coupling this genomic resource with external measurements from breed standards and individuals as well as skeletal measurements from museum specimens, we identify 51 regions of the dog genome associated with phenotypic variation among breeds in 57 traits. The complex traits include average breed body size and external body dimensions and cranial, dental, and long bone shape and size with and without allometric scaling. In contrast to the results from association mapping of quantitative traits in humans and domesticated plants, we find that across dog breeds, a small number of quantitative trait loci (≤3) explain the majority of phenotypic variation for most of the traits we studied. In addition, many genomic regions show signatures of recent selection, with most of the highly differentiated regions being associated with breed-defining traits such as body size, coat characteristics, and ear floppiness. Our results demonstrate the efficacy of mapping multiple traits in the domestic dog using a database of genotyped individuals and highlight the important role human-directed selection has played in altering the genetic architecture of key traits in this important species.
study  biodet  sapiens  embodied  GWAS  genetics  multi  regularizer  QTL  sex  developmental  genetic-load  evopsych  null-result  nature  model-organism  genomics  twitter  social  scitariat  discussion  publishing  realness  drama  preprint  debate  critique  news  org:mag  org:sci  org:biz 
april 2017 by nhaliday
Surnames: a New Source for the History of Social Mobility
This paper explains how surname distributions can be used as a way to
measure rates of social mobility in contemporary and historical societies.
This allows for estimates of social mobility rates for any population for which the distribution of surnames overall is known as well as the distribution of surnames among some elite or underclass. Such information exists, for example, for England back to 1300, and for Sweden back to 1700. However surname distributions reveal a different, more fundamental type of mobility than that conventionally estimated. Thus surname estimates also allow for measuring a different aspect of social mobility, but the aspect that matters for mobility of social groups, and for families in the long run.

The Big Sort: Selective Migration and the Decline of Northern England, 1800-2017: http://migrationcluster.ucdavis.edu/events/seminars_2015-2016/sem_assets/clark/paper_clark_northern-disadvantage.pdf
The north of England in recent years has been poorer, less healthy, less educated and slower growing than the south. Using two sources - surnames that had a different regional distribution in England in the 1840s, and a detailed genealogy of 78,000 people in England giving birth and death locations - we show that the decline of the north is mainly explained by selective outmigration of the educated and talented.

Genetic Consequences of Social Stratification in Great Britain: https://www.biorxiv.org/content/biorxiv/early/2018/10/30/457515
pdf  study  spearhead  gregory-clark  economics  cliometrics  status  class  mobility  language  methodology  metrics  natural-experiment  🎩  tricks  history  early-modern  britain  china  asia  path-dependence  europe  nordic  pro-rata  higher-ed  elite  success  society  legacy  stylized-facts  age-generation  broad-econ  s-factor  measurement  within-group  pop-structure  flux-stasis  microfoundations  multi  shift  mostly-modern  migration  biodet  endo-exo  behavioral-gen  regression-to-mean  human-capital  education  oxbridge  endogenous-exogenous  ideas  bio  preprint  genetics  genomics  GWAS 
march 2017 by nhaliday
An anatomically comprehensive atlas of the adult human brain transcriptome
In each brain independently, 84% of unique transcripts on the microarrays (29,412, referred to as genes for this manuscript) were found to be expressed in at least one structure (91.4% overlap in expressed gene sets between brains), consistent with the percentage of genes expressed in mouse brain by ISH (80%; ref. 1) and fetal human brain by microarrays (76%; ref. 11).
study  bio  sapiens  biodet  genetics  genomics  neuro  model-organism  comparison  GWAS  🌞  neuro-nitgrit 
march 2017 by nhaliday
Epidemiology, epigenetics and the ‘Gloomy Prospect’: embracing randomness in population health research and practice | International Journal of Epidemiology | Oxford Academic
Despite successes in identifying causes, it is often claimed that there are missing additional causes for even reasonably well-understood conditions such as lung cancer and coronary heart disease. Several lines of evidence suggest that largely chance events, from the biographical down to the sub-cellular, contribute an important stochastic element to disease risk that is not epidemiologically tractable at the individual level. Epigenetic influences provide a fashionable contemporary explanation for such seemingly random processes. Chance events—such as a particular lifelong smoker living unharmed to 100 years—are averaged out at the group level. As a consequence population-level differences (for example, secular trends or differences between administrative areas) can be entirely explicable by causal factors that appear to account for only a small proportion of individual-level risk. In public health terms, a modifiable cause of the large majority of cases of a disease may have been identified, with a wild goose chase continuing in an attempt to discipline the random nature of the world with respect to which particular individuals will succumb.

choice quote:
"With the perception (in my view exaggerated) that genome-wide association studies (GWASs) have failed to deliver on initial expectations,5 the next phase of enhanced risk prediction will certainly shift to ‘epigenetics’6,7—the currently fashionable response to any question to which you do not know the answer."
study  bio  medicine  genetics  genomics  sib-study  twin-study  cancer  cardio  essay  variance-components  signal-noise  random  causation  roots  gwern  explanation  methodology  🌞  biodet  QTL  correlation  epigenetics  GWAS  epidemiology  big-picture  public-health  composition-decomposition 
march 2017 by nhaliday
The genetics of politics: discovery, challenges, and progress
Figure 1. Summary of relative genetic and environmental influences on political traits.

- heritability increases discontinuously on leaving home
- pretty big range of heritability for different particular traits (party identification is lowest w/ largest shared environment by far)
- overall ideology quite highly heritable
- social trust is surprisingly highly compared other measurements I've seen...
- ethnocentrism quite low (sample-dependent?)
- authoritarianism and traditionalism quite high
- voter turnout quite high

Genes, psychological traits and civic engagement: http://rstb.royalsocietypublishing.org/content/370/1683/20150015
We show an underlying genetic contribution to an index of civic engagement (0.41), as well as for the individual acts of engagement of volunteering for community or public service activities (0.33), regularly contributing to charitable causes (0.28) and voting in elections (0.27). There are closer genetic relationships between donating and the other two activities; volunteering and voting are not genetically correlated. Further, we show that most of the correlation between civic engagement and both positive emotionality and verbal IQ can be attributed to genes that affect both traits.

Are Political Orientations Genetically Transmitted?: http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1006&context=poliscifacpub
TABLE 1. Genetic and Environmental Influences on Political Attitudes: The 28 Individual Wilson–Patterson Items

The origins of party identification and its relationship to political orientations: http://sci-hub.tw/http://www.sciencedirect.com/science/article/pii/S0191886915002470

All models showed a good overall fit (see Table 3). The data indicate that party identification is substantially heritable, with about 50% of the variation in PID attributable to additive genetic effects. Moreover, the results indicate that the non-genetic influences on party identification stem primarily from unique environmental factors rather than shared ones such as growing up in the same family. This too is not consistent with the Michigan model.

Table 3 also indicates that genetic influences explained about 50% of the variance in liberalism–conservatism. This estimate is similar to previous behavior genetic findings on political attitudes (e.g., Alford et al., 2005; Bouchard, 2004; Hatemi et al., 2014; Kandler, Bleidorn, & Riemann, 2012). The remaining variance was again due primarily to nonshared environmental influences. The latter finding indicates that the Michigan hypothesis that partisan social influences affect political orientations may have some merit, although the substantial level of heritability for this variable suggests that genetic effects also play an important role.

...

As Table 4 reveals, the best fitting model indicates that 100% of the genetic variance in PID is held in common with liberalism–conservatism ([aC2]/[aC2 + aPID2] = 1.00). Similarly, 73% of the environmental variation in PID is shared with liberalism–conservatism ([eC2]/[eC2 + ePID2] = .73). All told, only 13% of the total variance in PID cannot be explained by variation in liberalism–conservatism (1 [aC2 + eC2] = .13), as illustrated in Fig. 3. Since only a small proportion of the variance in PID cannot be explained by liberalism– conservatism, the findings are consistent with the hypothesis that genetic and environmental factors influence liberalism–conservatism, which in turn affects party identification. However, as discussed below, other causal scenarios cannot be ruled out.

Table 4 and Fig. 3 also show that 55% of the total variance in liberalism–conservatism cannot be accounted for by variance in PID

Fig. 3. Venn diagram mapping the common and specific variance in party
identification and liberalism–conservatism.

intuition for how you can figure out overlap of variance: look at how corr(PID, liberal-conservative) differs between MZ and DZ twin pairs, etc., fit structural equational model

p_k,i,j = r_A a_k,i,j,p + r_C c_k,i,p + r_E e_k,i,j,p (k=MZ or DZ, i=1..n_k, j=1,2, p=PID or LC value)

c_k,i,j,p = r_{C,p} c'_k,i,p + r_{C,common} c'_k,i,common (ditto)
e_k,i,j,p = r_{E,p} e'_k,i,j,p + r_{E,common} e'_k,i,j,common (ditto)

MZ twins:
a_MZ,i,j,p = r_{A,p} a'_MZ,i,p + r_{A,common} a'_MZ,i,common (i=1..n_k, j=1,2 p=PID or LC value)

DZ twins:
a_DZ,i,j,p = r_{A,p} (1/2 a'_DZ,i,p + 1/2 a'_DZ,i,j,p) + r_{A,common} (1/2 a'_DZ,i,common + 1/2 a'_DZ,i,j,common) (i=1..n_k, j=1,2 p=PID or LC value)

Gaussian distribution for the underlying a', c' and e' variables, maximum likelihood, etc.

see page 9 here: https://pinboard.in/u:nhaliday/b:70f8b5b559a9

basically:
1. calculate population means μ from data (so just numbers)
2. calculate covariance matrix Σ in terms of latent parameters r_A, r_C, etc. (so variable correlations)
3. assume observed values are Gaussian with those parameters μ, Σ
4. maximum likelihood to figure out the parameters r_A, r_C, etc.

A Genetic Basis of Economic Egalitarianism: http://sci-hub.tw/10.1007/s11211-017-0297-y
Our results show that the large portion of the variance in a four-item economic egalitarianism scale can be attributed to genetic factor. At the same time, shared environment, as a socializing factor, has no significant effect. The effect of environment seems to be fully reserved for unique personal experience. Our findings further problematize a long-standing view that social justice attitudes are dominantly determined by socialization.

published in the journal "Social Justice Research" by some Hungarians, lol

various political science findings, w/ a few behavioral genetic, focus on Trump, right-wing populism/authoritarianism, and polarization: http://www.nationalaffairs.com/blog/detail/findings-a-daily-roundup/a-bridge-too-far
pdf  study  org:nat  biodet  politics  values  psychology  social-psych  genetics  variance-components  survey  meta-analysis  environmental-effects  🌞  parenting  replication  candidate-gene  GWAS  anthropology  society  trust  hive-mind  tribalism  authoritarianism  things  sociology  expression-survival  civic  shift  ethnocentrism  spearhead  garett-jones  broad-econ  political-econ  behavioral-gen  biophysical-econ  polisci  stylized-facts  neuro-nitgrit  phalanges  identity-politics  tradition  microfoundations  ideology  multi  genetic-correlation  data  database  twin-study  objektbuch  gender  capitalism  peace-violence  military  labor  communism  migration  civil-liberty  exit-voice  censorship  sex  sexuality  assortative-mating  usa  anglo  comparison  knowledge  coalitions  piracy  correlation  intersection  latent-variables  methodology  stats  models  ML-MAP-E  nibble  explanation  bioinformatics  graphical-models  hypothesis-testing  intersection-connectedness  poll  egalitarianism-hierarchy  envy  inequality  justice  westminster  publishing 
february 2017 by nhaliday
Friendship and natural selection
More than any other species, humans form social ties to individuals who are neither kin nor mates, and these ties tend to be with similar people. Here, we show that this similarity extends to genotypes. Across the whole genome, friends’ genotypes at the single nucleotide polymorphism level tend to be positively correlated (homophilic). In fact, the increase in similarity relative to strangers is at the level of fourth cousins. However, certain genotypes are also negatively correlated (heterophilic) in friends. And the degree of correlation in genotypes can be used to create a “friendship score” that predicts the existence of friendship ties in a hold-out sample. A focused gene-set analysis indicates that some of the overall correlation in genotypes can be explained by specific systems; for example, an olfactory gene set is homophilic and an immune system gene set is heterophilic, suggesting that these systems may play a role in the formation or maintenance of friendship ties. Friends may be a kind of “functional kin.” Finally, homophilic genotypes exhibit significantly higher measures of positive selection, suggesting that, on average, they may yield a synergistic fitness advantage that has been helping to drive recent human evolution.
study  psychology  social-psych  anthropology  genetics  genomics  biodet  correlation  genetic-correlation  🌞  GWAS  sociology  org:nat 
february 2017 by nhaliday
Comparing the Developmental Genetics of Cognition and Personality over the Lifespan
- Tucker-Drob

Both cognition and personality are moderately heritable and exhibit large increases in stability with age; however, marked differences are evident. First, the heritability of cognition increases substantially with child age, while the heritability of personality decreases modestly with age. Second, increasing stability of cognition with age is overwhelmingly mediated by genetic factors, whereas increasing stability of personality with age is entirely mediated by environmental factors. Third, the maturational time-course of stability differs: Stability of cognition nears its asymptote by the end of the first decade of life, whereas stability of personality takes three decades to near its asymptote.

Theoretical Concepts in the Genetics of Personality Development: http://labs.la.utexas.edu/tucker-drob/files/2015/02/Tucker-Drob-Briley-Genetics-of-Personality-Development-Chapter.pdf
pdf  study  survey  biodet  genetics  iq  personality  variance-components  aging  developmental  QTL  GxE  🌞  meta-analysis  GWAS  comparison  correlation  behavioral-gen  flexibility  sequential  chart  longitudinal  flux-stasis  article  spearhead  multi  essay  methodology  explanation  volo-avolo  intricacy 
february 2017 by nhaliday
Holocene selection for variants associated with cognitive ability: Comparing ancient and modern genomes. | bioRxiv
- Michael Woodley

https://news.ycombinator.com/item?id=13759949

Human populations living in Eurasia during the Holocene experienced significant evolutionary change. It has been predicted that the transition of Holocene populations into agrarianism and urbanization brought about culture-gene co-evolution that favoured via directional selection genetic variants associated with higher general cognitive ability (GCA).
...
These observations are consistent with the expectation that GCA rose during the Holocene.
study  preprint  bio  sapiens  genetics  genomics  GWAS  antiquity  trends  iq  dysgenics  recent-selection  aDNA  multi  hn  commentary  gwern  enhancement  evolution  blowhards  behavioral-gen 
february 2017 by nhaliday
Prevalence and architecture of de novo mutations in developmental disorders : Nature
We estimate that 42% of our cohort carry pathogenic DNMs in coding sequences; approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that developmental disorders caused by DNMs have an average prevalence of 1 in 213 to 1 in 448 births, depending on parental age. Given current global demographics, this equates to almost 400,000 children born per year.
pdf  study  org:nat  genetics  genomics  genetic-load  paternal-age  hmm  developmental  parenting  aging  biodet  GWAS  🌞  👽  science-anxiety  autism  epidemiology  deep-materialism  public-health  rot 
february 2017 by nhaliday
INFECTIOUS CAUSATION OF DISEASE: AN EVOLUTIONARY PERSPECTIVE
A New Germ Theory: https://www.theatlantic.com/magazine/archive/1999/02/a-new-germ-theory/377430/
The dictates of evolution virtually demand that the causes of some of humanity's chronic and most baffling "noninfectious" illnesses will turn out to be pathogens -- that is the radical view of a prominent evolutionary biologist

A LATE-SEPTEMBER heat wave enveloped Amherst College, and young people milled about in shorts or sleeveless summer frocks, or read books on the grass. Inside the red-brick buildings framing the leafy quadrangle students listened to lectures on Ellison and Emerson, on Paul Verlaine and the Holy Roman Empire. Few suspected that strains of the organism that causes cholera were growing nearby, in the Life Sciences Building. If they had known, they would probably not have grasped the implications. But these particular strains of cholera make Paul Ewald smile; they are strong evidence that he is on the right track. Knowing the rules of evolutionary biology, he believes, can change the course of infectious disease.

https://www.theatlantic.com/past/docs/issues/99feb/germ2.htm
I HAVE a motto," Gregory Cochran told me recently. "'Big old diseases are infectious.' If it's common, higher than one in a thousand, I get suspicious. And if it's old, if it has been around for a while, I get suspicious."

https://www.theatlantic.com/past/docs/issues/99feb/germ3.htm
pdf  study  speculation  bio  evolution  sapiens  parasites-microbiome  red-queen  disease  west-hunter  🌞  unit  nibble  len:long  biodet  EGT  wild-ideas  big-picture  epidemiology  deep-materialism  🔬  spearhead  scitariat  maxim-gun  ideas  lens  heterodox  darwinian  equilibrium  medicine  heuristic  spreading  article  psychiatry  QTL  distribution  behavioral-gen  genetics  population-genetics  missing-heritability  gender  sex  sexuality  cardio  track-record  aging  popsci  natural-experiment  japan  asia  meta:medicine  profile  ability-competence  empirical  theory-practice  data  magnitude  scale  cost-benefit  is-ought  occam  parsimony  stress  GWAS  roots  explanans  embodied  obesity  geography  canada  britain  anglo  trivia  cocktail  shift  aphorism  stylized-facts  evidence  inference 
february 2017 by nhaliday
Genetics and educational attainment | npj Science of Learning
Figure 1 is quite good
Sibling Correlations for Behavioral Traits. This figure displays sibling correlations for five traits measured in a large sample of Swedish brother pairs born 1951–1970. All outcomes except years of schooling are measured at conscription, around the age of 18.

correlations for IQ/EA for adoptees are actually nontrivial in adulthood, hmm

Figure 2 has GWAS R^2s through 2016 (in-sample, I guess?)
study  org:nat  biodet  education  methodology  essay  survey  genetics  GWAS  variance-components  init  causation  🌞  metrics  population-genetics  explanation  unit  nibble  len:short  big-picture  behavioral-gen  state-of-art  iq  embodied  correlation  twin-study  sib-study  summary  europe  nordic  data  visualization  s:*  tip-of-tongue  spearhead  bioinformatics 
february 2017 by nhaliday
Association of the Dopamine D4 Receptor (DRD4) Gene and Approach-Related Personality Traits: Meta-Analysis and New Data - Biological Psychiatry
Our initial meta-analysis supported the association of the DRD4 C-521T polymorphism, but not the VNTR polymorphism, with approach-related traits. This conclusion was qualified by evidence of significant publication bias and the failure to detect association in a replication sample comprising individuals at the extremes of the trait distribution. The association of the C-521T polymorphism observed in our initial meta-analysis was robust to the inclusion of these new data, but our revised meta-analysis indicated that the association was present for measures of novelty seeking and impulsivity but not for measures of extraversion.

Meta-analysis of the heterogeneity in association of DRD4 7-repeat allele and AD/HD: stronger association with AD/HD combined type: https://www.ncbi.nlm.nih.gov/pubmed/20468072

Molecular Psychiatry - High prevalence of rare dopamine receptor D4 alleles in children diagnosed with attention-deficit hyperactivity disorder: http://www.nature.com/mp/journal/v8/n5/full/4001350a.html
study  meta-analysis  biodet  psychology  cog-psych  neuro  genetics  replication  QTL  candidate-gene  personality  attention  neuro-nitgrit  behavioral-gen  extra-introversion  multi  disease  psychiatry  epidemiology  GWAS 
february 2017 by nhaliday
European Journal of Human Genetics - A systematic review of cancer GWAS and candidate gene meta-analyses reveals limited overlap but similar effect sizes
Our findings suggest that meta-analyses of well-conducted candidate gene studies may continue to add to our understanding of the genetic associations in the post-GWAS era.
study  org:nat  biodet  methodology  GWAS  meta-analysis  genetics  causation  science  genomics  candidate-gene 
february 2017 by nhaliday
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