nhaliday + population-genetics   167

Measuring fitness heritability: Life history traits versus morphological traits in humans - Gavrus‐Ion - 2017 - American Journal of Physical Anthropology - Wiley Online Library
Traditional interpretation of Fisher's Fundamental Theorem of Natural Selection is that life history traits (LHT), which are closely related with fitness, show lower heritabilities, whereas morphological traits (MT) are less related with fitness and they are expected to show higher heritabilities.

...

LHT heritabilities ranged from 2.3 to 34% for the whole sample, with men showing higher heritabilities (4–45%) than women (0‐23.7%). Overall, MT presented higher heritability values than most of LHT, ranging from 0 to 40.5% in craniofacial indices, and from 13.8 to 32.4% in craniofacial angles. LHT showed considerable additive genetic variance values, similar to MT, but also high environmental variance values, and most of them presenting a higher evolutionary potential than MT.
study  biodet  behavioral-gen  population-genetics  hmm  contrarianism  levers  inference  variance-components  fertility  life-history  demographics  embodied  prediction  contradiction  empirical  sib-study 
may 2019 by nhaliday
Who We Are | West Hunter
I’m going to review David Reich’s new book, Who We Are and How We Got Here. Extensively: in a sense I’ve already been doing this for a long time. Probably there will be a podcast. The GoFundMe link is here. You can also send money via Paypal (Use the donate button), or bitcoins to 1Jv4cu1wETM5Xs9unjKbDbCrRF2mrjWXr5. In-kind donations, such as orichalcum or mithril, are always appreciated.

This is the book about the application of ancient DNA to prehistory and history.

height difference between northern and southern europeans: https://westhunt.wordpress.com/2018/03/29/who-we-are-1/
mixing, genocide of males, etc.: https://westhunt.wordpress.com/2018/03/29/who-we-are-2-purity-of-essence/
rapid change in polygenic traits (appearance by Kevin Mitchell and funny jab at Brad Delong ("regmonkey")): https://westhunt.wordpress.com/2018/03/30/rapid-change-in-polygenic-traits/
schiz, bipolar, and IQ: https://westhunt.wordpress.com/2018/03/30/rapid-change-in-polygenic-traits/#comment-105605
Dan Graur being dumb: https://westhunt.wordpress.com/2018/04/02/the-usual-suspects/
prediction of neanderthal mixture and why: https://westhunt.wordpress.com/2018/04/03/who-we-are-3-neanderthals/
New Guineans tried to use Denisovan admixture to avoid UN sanctions (by "not being human"): https://westhunt.wordpress.com/2018/04/04/who-we-are-4-denisovans/
also some commentary on decline of Out-of-Africa, including:
"Homo Naledi, a small-brained homonin identified from recently discovered fossils in South Africa, appears to have hung around way later that you’d expect (up to 200,000 years ago, maybe later) than would be the case if modern humans had occupied that area back then. To be blunt, we would have eaten them."

Live Not By Lies: https://westhunt.wordpress.com/2018/04/08/live-not-by-lies/
Next he slams people that suspect that upcoming genetic genetic analysis will, in most cases, confirm traditional stereotypes about race – the way the world actually looks.

The people Reich dumps on are saying perfectly reasonable things. He criticizes Henry Harpending for saying that he’d never seen an African with a hobby. Of course, Henry had actually spent time in Africa, and that’s what he’d seen. The implication is that people in Malthusian farming societies – which Africa was not – were selected to want to work, even where there was no immediate necessity to do so. Thus hobbies, something like a gerbil running in an exercise wheel.

He criticized Nicholas Wade, for saying that different races have different dispositions. Wade’s book wasn’t very good, but of course personality varies by race: Darwin certainly thought so. You can see differences at birth. Cover a baby’s nose with a cloth: Chinese and Navajo babies quietly breathe through their mouth, European and African babies fuss and fight.

Then he attacks Watson, for asking when Reich was going to look at Jewish genetics – the kind that has led to greater-than-average intelligence. Watson was undoubtedly trying to get a rise out of Reich, but it’s a perfectly reasonable question. Ashkenazi Jews are smarter than the average bear and everybody knows it. Selection is the only possible explanation, and the conditions in the Middle ages – white-collar job specialization and a high degree of endogamy, were just what the doctor ordered.

Watson’s a prick, but he’s a great prick, and what he said was correct. Henry was a prince among men, and Nick Wade is a decent guy as well. Reich is totally out of line here: he’s being a dick.

Now Reich may be trying to burnish his anti-racist credentials, which surely need some renewal after having pointing out that race as colloquially used is pretty reasonable, there’s no reason pops can’t be different, people that said otherwise ( like Lewontin, Gould, Montagu, etc. ) were lying, Aryans conquered Europe and India, while we’re tied to the train tracks with scary genetic results coming straight at us. I don’t care: he’s being a weasel, slandering the dead and abusing the obnoxious old genius who laid the foundations of his field. Reich will also get old someday: perhaps he too will someday lose track of all the nonsense he’s supposed to say, or just stop caring. Maybe he already has… I’m pretty sure that Reich does not like lying – which is why he wrote this section of the book (not at all logically necessary for his exposition of the ancient DNA work) but the required complex juggling of lies and truth required to get past the demented gatekeepers of our society may not be his forte. It has been said that if it was discovered that someone in the business was secretly an android, David Reich would be the prime suspect. No Talleyrand he.

https://westhunt.wordpress.com/2018/04/12/who-we-are-6-the-americas/
The population that accounts for the vast majority of Native American ancestry, which we will call Amerinds, came into existence somewhere in northern Asia. It was formed from a mix of Ancient North Eurasians and a population related to the Han Chinese – about 40% ANE and 60% proto-Chinese. Is looks as if most of the paternal ancestry was from the ANE, while almost all of the maternal ancestry was from the proto-Han. [Aryan-Transpacific ?!?] This formation story – ANE boys, East-end girls – is similar to the formation story for the Indo-Europeans.

https://westhunt.wordpress.com/2018/04/18/who-we-are-7-africa/
In some ways, on some questions, learning more from genetics has left us less certain. At this point we really don’t know where anatomically humans originated. Greater genetic variety in sub-Saharan African has been traditionally considered a sign that AMH originated there, but it possible that we originated elsewhere, perhaps in North Africa or the Middle East, and gained extra genetic variation when we moved into sub-Saharan Africa and mixed with various archaic groups that already existed. One consideration is that finding recent archaic admixture in a population may well be a sign that modern humans didn’t arise in that region ( like language substrates) – which makes South Africa and West Africa look less likely. The long-continued existence of homo naledi in South Africa suggests that modern humans may not have been there for all that long – if we had co-existed with homo naledi, they probably wouldn’t lasted long. The oldest known skull that is (probably) AMh was recently found in Morocco, while modern humans remains, already known from about 100,000 years ago in Israel, have recently been found in northern Saudi Arabia.

While work by Nick Patterson suggests that modern humans were formed by a fusion between two long-isolated populations, a bit less than half a million years ago.

So: genomics had made recent history Africa pretty clear. Bantu agriculuralists expanded and replaced hunter-gatherers, farmers and herders from the Middle East settled North Africa, Egypt and northeaat Africa, while Nilotic herdsmen expanded south from the Sudan. There are traces of earlier patterns and peoples, but today, only traces. As for questions back further in time, such as the origins of modern humans – we thought we knew, and now we know we don’t. But that’s progress.

https://westhunt.wordpress.com/2018/04/18/reichs-journey/
David Reich’s professional path must have shaped his perspective on the social sciences. Look at the record. He starts his professional career examining the role of genetics in the elevated prostate cancer risk seen in African-American men. Various social-science fruitcakes oppose him even looking at the question of ancestry ( African vs European). But they were wrong: certain African-origin alleles explain the increased risk. Anthropologists (and human geneticists) were sure (based on nothing) that modern humans hadn’t interbred with Neanderthals – but of course that happened. Anthropologists and archaeologists knew that Gustaf Kossina couldn’t have been right when he said that widespread material culture corresponded to widespread ethnic groups, and that migration was the primary explanation for changes in the archaeological record – but he was right. They knew that the Indo-European languages just couldn’t have been imposed by fire and sword – but Reich’s work proved them wrong. Lots of people – the usual suspects plus Hindu nationalists – were sure that the AIT ( Aryan Invasion Theory) was wrong, but it looks pretty good today.

Some sociologists believed that caste in India was somehow imposed or significantly intensified by the British – but it turns out that most jatis have been almost perfectly endogamous for two thousand years or more…

It may be that Reich doesn’t take these guys too seriously anymore. Why should he?

varnas, jatis, aryan invastion theory: https://westhunt.wordpress.com/2018/04/22/who-we-are-8-india/

europe and EEF+WHG+ANE: https://westhunt.wordpress.com/2018/05/01/who-we-are-9-europe/

https://www.nationalreview.com/2018/03/book-review-david-reich-human-genes-reveal-history/
The massive mixture events that occurred in the recent past to give rise to Europeans and South Asians, to name just two groups, were likely “male mediated.” That’s another way of saying that men on the move took local women as brides or concubines. In the New World there are many examples of this, whether it be among African Americans, where most European ancestry seems to come through men, or in Latin America, where conquistadores famously took local women as paramours. Both of these examples are disquieting, and hint at the deep structural roots of patriarchal inequality and social subjugation that form the backdrop for the emergence of many modern peoples.
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march 2018 by nhaliday
Altruism in a volatile world | Nature
The evolution of altruism—costly self-sacrifice in the service of others—has puzzled biologists1 since The Origin of Species. For half a century, attempts to understand altruism have developed around the concept that altruists may help relatives to have extra offspring in order to spread shared genes2. This theory—known as inclusive fitness—is founded on a simple inequality termed Hamilton’s rule2. However, explanations of altruism have typically not considered the stochasticity of natural environments, which will not necessarily favour genotypes that produce the greatest average reproductive success3,4. Moreover, empirical data across many taxa reveal associations between altruism and environmental stochasticity5,6,7,8, a pattern not predicted by standard interpretations of Hamilton’s rule. Here we derive Hamilton’s rule with explicit stochasticity, leading to new predictions about the evolution of altruism. We show that altruists can increase the long-term success of their genotype by reducing the temporal variability in the number of offspring produced by their relatives. Consequently, costly altruism can evolve even if it has a net negative effect on the average reproductive success of related recipients. The selective pressure on volatility-suppressing altruism is proportional to the coefficient of variation in population fitness, and is therefore diminished by its own success. Our results formalize the hitherto elusive link between bet-hedging and altruism4,9,10,11, and reveal missing fitness effects in the evolution of animal societies.
study  bio  evolution  altruism  kinship  stylized-facts  models  intricacy  random  signal-noise  time  order-disorder  org:nat  EGT  cooperate-defect  population-genetics  moments  expectancy  multiplicative  additive 
march 2018 by nhaliday
Why Sex? And why only in Pairs? - Marginal REVOLUTION
The core conclusion is that mutations continue to rise with the number of sex-participating partners, but in simple Red Queen models the limiting features of the genotypes is the same whether there are two, three, or more partners.

Men Are Animals: http://www.overcomingbias.com/2018/06/men-are-animals.html
I agree with all the comments citing motility/sessility.
econotariat  marginal-rev  commentary  study  summary  economics  broad-econ  interdisciplinary  bio  biodet  deep-materialism  new-religion  eden  gender  sex  EGT  explanans  red-queen  parasites-microbiome  mutation  comparison  evolution  roots  🌞  population-genetics  genetics  marginal  equilibrium  number  ecology  whole-partial-many  uniqueness  parsimony  multi  cost-benefit  outcome-risk  uncertainty  moments  spatial  travel  explore-exploit  ratty  hanson 
january 2018 by nhaliday
A genetic map of the world – Gene Expression
The above map is from a new preprint on the patterns of genetic variation as a function of geography for humans, Genetic landscapes reveal how human genetic diversity aligns with geography. The authors assemble an incredibly large dataset to generate these figures. The orange zones are “troughs” of gene flow. Basically barriers to gene flow.  It is no great surprise that so many of the barriers correlate with rivers, mountains, and deserts. But the aim of this sort of work seems to be to make precise and quantitative intuitions which are normally expressed verbally.
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december 2017 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
Open Thread, 11/26/2017 – Gene Expression
A few days ago there was a Twitter thing about top five books that have influenced you. It’s hard for me to name five, but I put three books down for three different reasons:

- Principles of Population Genetics, because it gives you a model for how to analyze and understand evolutionary processes. There are other books out there besides Principles of Population Genetics. But if you buy this book you don’t need to buy another (at SMBE this year I confused Andy Clark with Mike Lynch for a second when introducing myself. #awkward)
- The Fall of Rome. A lot of historical writing can be tendentious. I’ve also noticed an unfortunate tendency of historians dropping into contemporary arguments and pretty much lying through omission or elision to support their political side (it usually goes “actually, I’m a specialist in this topic and my side is 100% correct because of obscure-stuff where I’m shading the facts”). The Fall of Rome illustrates the solidity that an archaeological and materialist take can give the field. This sort of materialism isn’t the final word, but it needs to be the start of the conversation.
- From Dawn to Decadence: 1500 to the Present: 500 Years of Western Cultural Life. To know things is important in and of itself. My own personal experience is that the returns to knowing things in a particular domain or area do not exhibit a linear return. Rather, it exhibits a logistic curve. Initially, it’s hard to make sense of anything from the facts, but at some point comprehension and insight increase rapidly, until you reach the plateau of diminishing marginal returns.

If you haven’t, I recommend you subscribe to Patrick Wyman’s Tides of History podcast. I pretty much wait now for every new episode.
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november 2017 by nhaliday
Ancient Admixture in Human History
- Patterson, Reich et al., 2012
Population mixture is an important process in biology. We present a suite of methods for learning about population mixtures, implemented in a software package called ADMIXTOOLS, that support formal tests for whether mixture occurred and make it possible to infer proportions and dates of mixture. We also describe the development of a new single nucleotide polymorphism (SNP) array consisting of 629,433 sites with clearly documented ascertainment that was specifically designed for population genetic analyses and that we genotyped in 934 individuals from 53 diverse populations. To illustrate the methods, we give a number of examples that provide new insights about the history of human admixture. The most striking finding is a clear signal of admixture into northern Europe, with one ancestral population related to present-day Basques and Sardinians and the other related to present-day populations of northeast Asia and the Americas. This likely reflects a history of admixture between Neolithic migrants and the indigenous Mesolithic population of Europe, consistent with recent analyses of ancient bones from Sweden and the sequencing of the genome of the Tyrolean “Iceman.”
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november 2017 by nhaliday
SEXUAL DIMORPHISM, SEXUAL SELECTION, AND ADAPTATION IN POLYGENIC CHARACTERS - Lande - 1980 - Evolution - Wiley Online Library
https://twitter.com/gcochran99/status/970758341990367232
https://archive.is/mcKvr
Lol, that's nothing, my biology teacher in high school told me sex differences couldn't evolve since all of us inherit 50% of genes from parents of both sexes. Being a raucous hispanic kid I burst out laughing, she was not pleased
--
Sex differences actually evolve more slowly because of that: something like 80 times more slowly.
...
Doesn't have that number, but in the same ballpark.

Sexual Dimorphism, Sexual Selection, And Adaptation In Polygenic Characters

Russell Lande

https://twitter.com/gcochran99/status/999189778867208193
https://archive.is/AR8FY
I believe it, because sex differences [ in cases where the trait is not sex-limited ] evolve far more slowly than other things, on the order of 100 times more slowly. Lande 1980: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1558-5646.1980.tb04817.x

The deep past has a big vote in such cases.
...
as for the extent that women were voluntarily choosing mates 20k years ago, or 100k years ago - I surely don't know.

other time mentioned: https://pinboard.in/u:nhaliday/b:3a7c5b42dd50
study  article  bio  biodet  gender  gender-diff  evolution  genetics  population-genetics  methodology  nibble  sex  🌞  todo  pdf  piracy  marginal  comparison  pro-rata  data  multi  twitter  social  discussion  backup  west-hunter  scitariat  farmers-and-foragers  sexuality  evopsych  EEA 
november 2017 by nhaliday
Genetic influences on measures of the environment: a systematic review | Psychological Medicine | Cambridge Core
Background. Traditional models of psychiatric epidemiology often assume that the relationship between individuals and their environment is unidirectional, from environment to person. Accumulating evidence from developmental and genetic studies has made this perspective increasingly untenable.

Results. We identified 55 independent studies organized into seven categories: general and specific stressful life events (SLEs), parenting as reported by child, parenting reported by parent, family environment, social support, peer interactions, and marital quality. Thirty-five environmental measures in these categories were examined by at least two studies and produced weighted heritability estimates ranging from 7% to 39%, with most falling between 15% and 35%. The weighted heritability for all environmental measures in all studies was 27%. The weighted heritability for environmental measures by rating method was: self-report 29%, informant report 26%, and direct rater or videotape observation (typically examining 10 min of behavior) 14%.
study  meta-analysis  biodet  behavioral-gen  genetics  population-genetics  🌞  regularizer  environmental-effects  GxE  psychiatry  epidemiology  composition-decomposition 
october 2017 by nhaliday
Medicine as a pseudoscience | West Hunter
The idea that venesection was a good thing, or at least not so bad, on the grounds that one in a few hundred people have hemochromatosis (in Northern Europe) reminds me of the people who don’t wear a seatbelt, since it would keep them from being thrown out of their convertible into a waiting haystack, complete with nubile farmer’s daughter. Daughters. It could happen. But it’s not the way to bet.

Back in the good old days, Charles II, age 53, had a fit one Sunday evening, while fondling two of his mistresses.

Monday they bled him (cupping and scarifying) of eight ounces of blood. Followed by an antimony emetic, vitriol in peony water, purgative pills, and a clyster. Followed by another clyster after two hours. Then syrup of blackthorn, more antimony, and rock salt. Next, more laxatives, white hellebore root up the nostrils. Powdered cowslip flowers. More purgatives. Then Spanish Fly. They shaved his head and stuck blistering plasters all over it, plastered the soles of his feet with tar and pigeon-dung, then said good-night.

...

Friday. The king was worse. He tells them not to let poor Nelly starve. They try the Oriental Bezoar Stone, and more bleeding. Dies at noon.

Most people didn’t suffer this kind of problem with doctors, since they never saw one. Charles had six. Now Bach and Handel saw the same eye surgeon, John Taylor – who blinded both of them. Not everyone can put that on his resume!

You may wonder how medicine continued to exist, if it had a negative effect, on the whole. There’s always the placebo effect – at least there would be, if it existed. Any real placebo effect is very small: I’d guess exactly zero. But there is regression to the mean. You see the doctor when you’re feeling worse than average – and afterwards, if he doesn’t kill you outright, you’re likely to feel better. Which would have happened whether you’d seen him or not, but they didn’t often do RCTs back in the day – I think James Lind was the first (1747).

Back in the late 19th century, Christian Scientists did better than others when sick, because they didn’t believe in medicine. For reasons I think mistaken, because Mary Baker Eddy rejected the reality of the entire material world, but hey, it worked. Parenthetically, what triggered all that New Age nonsense in 19th century New England? Hash?

This did not change until fairly recently. Sometime in the early 20th medicine, clinical medicine, what doctors do, hit break-even. Now we can’t do without it. I wonder if there are, or will be, other examples of such a pile of crap turning (mostly) into a real science.

good tweet: https://twitter.com/bowmanthebard/status/897146294191390720
The brilliant GP I've had for 35+ years has retired. How can I find another one who meets my requirements?

1 is overweight
2 drinks more than officially recommended amounts
3 has an amused, tolerant atitude to human failings
4 is well aware that we're all going to die anyway, & there are better or worse ways to die
5 has a healthy skeptical attitude to mainstream medical science
6 is wholly dismissive of "a|ternative” medicine
7 believes in evolution
8 thinks most diseases get better without intervention, & knows the dangers of false positives
9 understands the base rate fallacy

EconPapers: Was Civil War Surgery Effective?: http://econpapers.repec.org/paper/htrhcecon/444.htm
contra Greg Cochran:
To shed light on the subject, I analyze a data set created by Dr. Edmund Andrews, a Civil war surgeon with the 1st Illinois Light Artillery. Dr. Andrews’s data can be rendered into an observational data set on surgical intervention and recovery, with controls for wound location and severity. The data also admits instruments for the surgical decision. My analysis suggests that Civil War surgery was effective, and increased the probability of survival of the typical wounded soldier, with average treatment effect of 0.25-0.28.

Medical Prehistory: https://westhunt.wordpress.com/2016/03/14/medical-prehistory/
What ancient medical treatments worked?

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76878
In some very, very limited conditions, bleeding?
--
Bad for you 99% of the time.

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76947
Colchicine – used to treat gout – discovered by the Ancient Greeks.

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76973
Dracunculiasis (Guinea worm)
Wrap the emerging end of the worm around a stick and slowly pull it out.
(3,500 years later, this remains the standard treatment.)
https://en.wikipedia.org/wiki/Ebers_Papyrus

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76971
Some of the progress is from formal medicine, most is from civil engineering, better nutrition ( ag science and physical chemistry), less crowded housing.

Nurses vs doctors: https://westhunt.wordpress.com/2014/10/01/nurses-vs-doctors/
Medicine, the things that doctors do, was an ineffective pseudoscience until fairly recently. Until 1800 or so, they were wrong about almost everything. Bleeding, cupping, purging, the four humors – useless. In the 1800s, some began to realize that they were wrong, and became medical nihilists that improved outcomes by doing less. Some patients themselves came to this realization, as when Civil War casualties hid from the surgeons and had better outcomes. Sometime in the early 20th century, MDs reached break-even, and became an increasingly positive influence on human health. As Lewis Thomas said, medicine is the youngest science.

Nursing, on the other hand, has always been useful. Just making sure that a patient is warm and nourished when too sick to take care of himself has helped many survive. In fact, some of the truly crushing epidemics have been greatly exacerbated when there were too few healthy people to take care of the sick.

Nursing must be old, but it can’t have existed forever. Whenever it came into existence, it must have changed the selective forces acting on the human immune system. Before nursing, being sufficiently incapacitated would have been uniformly fatal – afterwards, immune responses that involved a period of incapacitation (with eventual recovery) could have been selectively favored.

when MDs broke even: https://westhunt.wordpress.com/2014/10/01/nurses-vs-doctors/#comment-58981
I’d guess the 1930s. Lewis Thomas thought that he was living through big changes. They had a working serum therapy for lobar pneumonia ( antibody-based). They had many new vaccines ( diphtheria in 1923, whopping cough in 1926, BCG and tetanus in 1927, yellow fever in 1935, typhus in 1937.) Vitamins had been mostly worked out. Insulin was discovered in 1929. Blood transfusions. The sulfa drugs, first broad-spectrum antibiotics, showed up in 1935.

DALYs per doctor: https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/
The disability-adjusted life year (DALY) is a measure of overall disease burden – the number of years lost. I’m wondering just much harm premodern medicine did, per doctor. How many healthy years of life did a typical doctor destroy (net) in past times?

...

It looks as if the average doctor (in Western medicine) killed a bunch of people over his career ( when contrasted with doing nothing). In the Charles Manson class.

Eventually the market saw through this illusion. Only took a couple of thousand years.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100741
That a very large part of healthcare spending is done for non-health reasons. He has a chapter on this in his new book, also check out his paper “Showing That You Care: The Evolution of Health Altruism” http://mason.gmu.edu/~rhanson/showcare.pdf
--
I ran into too much stupidity to finish the article. Hanson’s a loon. For example when he talks about the paradox of blacks being more sentenced on drug offenses than whites although they use drugs at similar rate. No paradox: guys go to the big house for dealing, not for using. Where does he live – Mars?

I had the same reaction when Hanson parroted some dipshit anthropologist arguing that the stupid things people do while drunk are due to social expectations, not really the alcohol.
Horseshit.

I don’t think that being totally unable to understand everybody around you necessarily leads to deep insights.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100744
What I’ve wondered is if there was anything that doctors did that actually was helpful and if perhaps that little bit of success helped them fool people into thinking the rest of it helped.
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Setting bones. extracting arrows: spoon of Diocles. Colchicine for gout. Extracting the Guinea worm. Sometimes they got away with removing the stone. There must be others.
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Quinine is relatively recent: post-1500. Obstetrical forceps also. Caesarean deliveries were almost always fatal to the mother until fairly recently.

Opium has been around for a long while : it works.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100839
If pre-modern medicine was indeed worse than useless – how do you explain no one noticing that patients who get expensive treatments are worse off than those who didn’t?
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were worse off. People are kinda dumb – you’ve noticed?
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My impression is that while people may be “kinda dumb”, ancient customs typically aren’t.
Even if we assume that all people who lived prior to the 19th century were too dumb to make the rational observation, wouldn’t you expect this ancient practice to be subject to selective pressure?
--
Your impression is wrong. Do you think that there some slick reason for Carthaginians incinerating their first-born?

Theodoric of York, bloodletting: https://www.youtube.com/watch?v=yvff3TViXmY

details on blood-letting and hemochromatosis: https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100746

Starting Over: https://westhunt.wordpress.com/2018/01/23/starting-over/
Looking back on it, human health would have … [more]
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august 2017 by nhaliday
Genetic Architectures | West Hunter
Dairy cattle eventually graduate to McDonalds, so there is some interest in the genetics of beef production in dairy breeds. There is course more interest in the genetics of beef production in beef breeds of cattle.

Usually you don’t find a single allele that makes a lot of difference, but in some beef breeds, there are myostatin mutations that result in a ridiculous-looking, ‘double-muscled’ beast. Homozygosity for myostatin mutations causes difficulties in birth, so it takes really strong selection for beef production to make a myostatin null common. I don’t think you ever see this in dairy breeds.

But, as it turns out, there is a deletion that is pretty common in some dairy breeds that significantly increases milk production while killing homozygotes before birth.

Breeds under weaker selection for single traits, your typical cow of the past, probably have neither.

The point is that the genetic architecture of a quantitative trait does not have to be the same in different populations of the same species. For example, I have the impression that height is not as highly polygenic in Pygmies as it is most other human populations. There’s a particular region on chromosome 3 that seems to influence height- you don’t see such a concentration in Europeans.
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august 2017 by nhaliday
Effective population size for advantageous mutations | West Hunter
So, with beneficial mutations, the effective population size is very different. Instead of being dominated by bottlenecks, it is more influenced by eras of large population size – more and more so as the selective advantage of the mutation increases. In the limit, if we imagine  mutations so advantageous that they spread  very rapidly, the effective population size approaches the population mean.
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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
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july 2017 by nhaliday
Alzheimers | West Hunter
Some disease syndromes almost have to be caused by pathogens – for example, any with a fitness impact (prevalence x fitness reduction) > 2% or so, too big to be caused by mutational pressure. I don’t think that this is the case for AD: it hits so late in life that the fitness impact is minimal. However, that hardly means that it can’t be caused by a pathogen or pathogens – a big fraction of all disease syndromes are, including many that strike in old age. That possibility is always worth checking out, not least because infectious diseases are generally easier to prevent and/or treat.

There is new work that strongly suggests that pathogens are the root cause. It appears that the amyloid is an antimicrobial peptide. amyloid-beta binds to invading microbes and then surrounds and entraps them. ‘When researchers injected Salmonella into mice’s hippocampi, a brain area damaged in Alzheimer’s, A-beta quickly sprang into action. It swarmed the bugs and formed aggregates called fibrils and plaques. “Overnight you see the plaques throughout the hippocampus where the bugs were, and then in each single plaque is a single bacterium,” Tanzi says. ‘

obesity and pathogens: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79757
not sure about this guy, but interesting: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79748
http://perfecthealthdiet.com/2010/06/is-alzheimer%E2%80%99s-caused-by-a-bacterial-infection-of-the-brain/

https://westhunt.wordpress.com/2016/12/13/the-twelfth-battle-of-the-isonzo/
All too often we see large, long-lasting research efforts that never produce, never achieve their goal.

For example, the amyloid hypothesis [accumulation of amyloid-beta oligomers is the cause of Alzheimers] has been dominant for more than 20 years, and has driven development of something like 15 drugs. None of them have worked. At the same time the well-known increased risk from APOe4 has been almost entirely ignored, even though it ought to be a clue to the cause.

In general, when a research effort has been spinning its wheels for a generation or more, shouldn’t we try something different? We could at least try putting a fraction of those research dollars into alternative approaches that have not yet failed repeatedly.

Mostly this applies to research efforts that at least wish they were science. ‘educational research’ is in a special class, and I hardly know what to recommend. Most of the remedial actions that occur to me violate one or more of the Geneva conventions.

APOe4 related to lymphatic system: https://en.wikipedia.org/wiki/Apolipoprotein_E

https://westhunt.wordpress.com/2012/03/06/spontaneous-generation/#comment-2236
Look,if I could find out the sort of places that I usually misplace my keys – if I did, which I don’t – I could find the keys more easily the next time I lose them. If you find out that practitioners of a given field are not very competent, it marks that field as a likely place to look for relatively easy discovery. Thus medicine is a promising field, because on the whole doctors are not terribly good investigators. For example, none of the drugs developed for Alzheimers have worked at all, which suggests that our ideas on the causation of Alzheimers are likely wrong. Which suggests that it may (repeat may) be possible to make good progress on Alzheimers, either by an entirely empirical approach, which is way underrated nowadays, or by dumping the current explanation, finding a better one, and applying it.

You could start by looking at basic notions of field X and asking yourself: How do we really know that? Is there serious statistical evidence? Does that notion even accord with basic theory? This sort of checking is entirely possible. In most of the social sciences, we don’t, there isn’t, and it doesn’t.

Hygiene and the world distribution of Alzheimer’s disease: Epidemiological evidence for a relationship between microbial environment and age-adjusted disease burden: https://academic.oup.com/emph/article/2013/1/173/1861845/Hygiene-and-the-world-distribution-of-Alzheimer-s

Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease: http://stm.sciencemag.org/content/8/340/340ra72

Fungus, the bogeyman: http://www.economist.com/news/science-and-technology/21676754-curious-result-hints-possibility-dementia-caused-fungal
Fungus and dementia
paper: http://www.nature.com/articles/srep15015

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors: https://advances.sciencemag.org/content/5/1/eaau3333
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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
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july 2017 by nhaliday
Dadly adaptations | West Hunter
If we understood how this works, we might find that individuals and populations vary in their propensity to show paternal care ( for genetic reasons). I would guess that paternal care was ancestral in modern humans, but it’s easy enough to lose something like this when selective pressures no longer favor it. Wolves have paternal care, but dogs have lost it.

This could have something to do with better health in married men. High testosterone levels aren’t cost-free.

It’s possible that various modern environmental factors interfere with the triggers for dadliness. That would hardly be surprising, since we don’t really know how they work.

All this has a number of interesting social implications. Let’s see how many of them you guys can spot.

Poles in the Tent: https://westhunt.wordpress.com/2013/07/09/poles-in-the-tent/
I’m considering a different question: what was the impact of men’s contribution on their children’s survival and fitness? That’s not quite the same as the number of calories contributed. Food is not a single undifferentiated quantity: it’s a category, including a number of different kinds that can’t be freely substituted for each other. Proteins, fats, and carbohydrates can all serve as fuel, but you need protein to build tissue. And amino acids, the building blocks of proteins, are not all fungible. Some we can’t synthesize (essential amino acids) others can only be synthesized from a limited set of precursors, etc. Edible plants often have suboptimal mixes of amino acids ( too many Qs, not enough Us) , but I’ve never heard of this being a problem with meat. Then you have to consider essential fatty acids, vitamins, and trace elements.

In principle, if high-quality protein were the long pole in the tent, male provisioning of meat, which we see in chimpanzees, might matter quite a bit more than you would think from the number of calories alone. I’m not say that is necessarily the case, but it might be, and it’s worth checking out.

Sexual selection vs job specialization: https://westhunt.wordpress.com/2017/10/02/sexual-selection-vs-job-specialization/
Pretty much every species is subject to sexual selection: heritable characteristics that lead to more mates or better mates can be favored by natural selection. Typically, sexual selection favors different strategies in males and females. Generally, males can gain fitness with increased mating opportunities, while females gain more from high-quality mates or mates that confer resources. Since the variance in reproduction is usually greater in males than females, sexual selection is usually stronger in males, although it exists and is significant in both sexes.

Usually, though, males and females of a given species have very similar ways of making a living. A male deer and a female deer both eat grass or arugula or whatever. Sexual selection may drive them to evolve in different directions, but finding something to eat mostly drives them in the same direction.

Humans are an exception. In the long past, men hunted and women gathered. The mix varied: in Arctic regions, men produce almost all the food (while women made and repaired gear, as well as raising children). In groups like the Bushmen, women produced most of the calories, but done rightly you would count more than calories: if most of the local plants had low protein or low-quality protein (wrong amino acid mix), meat from hunting could be important out of proportion to its caloric value.

This has been going for a long time, so there must have been selection for traits that aided provisioning ability in each sex. Those job-related selective pressures probably changed with time. For example, male strength may have become less valuable when the Bushmen developed poison arrows.

I was looking for an intelligent discussion of this question – but I ran into this and couldn’t force myself to read further: ” It should not simply be assumed that the exclusion of women from hunting rests upon “natural” physiological differences. ”

God give me strength.

https://westhunt.wordpress.com/2017/10/02/sexual-selection-vs-job-specialization/#comment-96323
What does Greg think about the “plows vs hoes” theory? (As seen here, although Sarah Constantin didn’t invent it.)

The claim is that some societies adopted farming (Europe, the Middle East, Asia) while some societies adopted horticulture (Oceana, sub-Saharan Africa, various primitive peoples) and that this had an affect on gender relations.

Basically: farming is backbreaking work, which favours males, giving them a lot of social capital. You end up with a patriarchal kind of society, where the men do stuff and the women are mostly valuable for raising offspring.

...

It’s kinda true, in places. There is a connection I haven’t seen explicated: the ‘hoe culture” has to have some factor keeping population density low, so that labor is scarcer than land. Tropical diseases like malaria might be part of that. Then again, crops like yams don’t store well, better to keep them in the ground until eating. That means it’s hard to tax people – easy with grain bins. No taxes -> no State – > high local violence. At times, VD may also help limit density, cf Africa’s ‘sterility belt’.

I am not a Moron: https://westhunt.wordpress.com/2017/11/03/i-am-not-a-moron/
So said Augustin Fuentes on Twitter, a few days ago. He’s the same guy that said “Genes don’t do anything by themselves; epigenetics and complex metabolic and developmental systems are at play in how bodies work. The roundworm C. elegans has about 20,000 genes while humans have about 23,000 genes, yet it is pretty obvious that humans are more than 15-percent more complex than roundworms. So while genes matter, they are only a small part of the whole evolutionary picture. Focusing just on DNA won’t get you anywhere.”

Fuentes was claiming that we don’t really know that, back in prehistory, men did most of the hunting while women gathered.

...

Someone (Will@Evolving _Moloch) criticized this as a good candidate for the most misleading paragraph ever written. The folly of youth! When you’ve been around as long as I have, sonny, you will realize how hard it is to set records for stupidity.

Fuente’s para is multidimensional crap, of course. People used to hunt animals like red deer, or bison, or eland: sometimes mammoths or rhinos. Big animals. Back in the day, our ancestors used stabbing spears, which go back at least half a million years. Stand-off weapons like atlatls, or bows, or JSOW, are relatively recent. Hunters took big risks & suffered frequent injuries. Men are almost twice as strong as women, particularly in upper-body strength, which is what matters in spear-chucking. They’re also faster, which can be very important which your ambush fails.
So men did the hunting. This isn’t complicated.

Which contemporary hunter-gather societies followed this pattern, had men do almost all of the big-game hunting? All of them.

...

Look, feminists aren’t happy with human nature, the one that actually exists and is the product of long-term evolutionary pressures. Too bad for them. When they say stuff like “It should not simply be assumed that the exclusion of women from hunting rests upon “natural” physiological differences. “, they just sound like fools.. ‘natural physiological differences” exist. They’re as obvious a punch in the kisser.

Suppose you wanted to construct a society with effective sexual equality – which is probably just a mistake, but suppose it. The most effective approach would surely entail knowing and taking into account how the world actually ticks. You’d be better off understanding that about 6,000 genes (out of 20,000) show significant expression differences between the sexes, than by pretending that we’re all the same. You would to make it so: by hook or by crook, by state force and genetic engineering.

Similarly, if you want to minimize war, pretending that people aren’t warlike is a poor start – about as sensible as fighting forest fires by pretending that trees aren’t flammable.

My advice to Augustin Fuentes, about not being a moron: show, don’t tell.

https://westhunt.wordpress.com/2017/11/03/i-am-not-a-moron/#comment-97721
Since DNA is the enduring part, the part that gets transmitted from one generation to the next, the part that contains the instructions/program that determine development and specify everything – he’s wrong. Stupid, like you. Well, to be fair, ignorant as well: there are technical aspects of genetics that Agustin Fuentes is unlikely to know anything about, things that are almost never covered in the typical education of an anthropologist. I doubt if he knows what a Fisher wave is, or anything about selfish genetic elements, or coalescent theory, or for that matter the breeder’s equation.

There are a number of complex technical subjects, things that at least some people understand: those people can do stuff that the man in the street can’t. In most cases, amateurs don’t jump in and pretend to know what’s going on. For example you don’t hear much concerning amateur opinions concerning detonation physics or group theory. But they’re happy to have opinions about natural selection, even though they know fuck-all about it.

https://twitter.com/FinchesofDarwin/status/922924692389818368
https://archive.is/AcBgh
"Significantly fewer females are present at hunts than males...females tend to appear at the hunting site once the capture has been made..."

“Women in Tech”: https://bloodyshovel.wordpress.com/2017/10/26/women-in-tech/
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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
POPULATION STRUCTURE AND QUANTITATIVE CHARACTERS
The variance of among-group variance is substantial and does not depend on the number of loci contributing to variance in the character. It is just as large for polygenic characters as for single loci with the same additive variance. This implies that one polygenic character contains exactly as much information about population relationships as one single-locus marker.

same is true of expectation apparently (so drift has same impact on polygenic and single-locus traits)
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may 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?
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may 2017 by nhaliday
None So Blind | West Hunter
There have been several articles in the literature claiming that the gene frequency of the 35delG allele of connexin-26, the most common allele causing deafness in Europeans, has doubled in the past 200 years, as a result of relaxed selection and assortative mating over that period.

That’s fucking ridiculous. I see people referencing this in journal articles and books. It’s mentioned in OMIM. But it’s pure nonsense.

https://westhunt.wordpress.com/2013/03/05/none-so-blind/#comment-10483
The only way you’re going to see such a high frequency of an effectively lethal recessive in a continental population is if it conferred a reproductive advantage in heterozygotes. The required advantage must have been as large as its gene frequency, something around 1-2%.

So it’s like sickle-cell.

Now, if you decreased the bad reproductive consequences of deafness, what would you expect to happen? Gradual increase, at around 1 or 2% a generation, if the carrier advantage held – but it probably didn’t. It was probably a defense against some infectious disease, and those have become much less important. If there was no longer any carrier advantage, the frequency wouldn’t change at all.

In order to double in 200 years, you would need a carrier advantage > 9%.

Assortative mating,deaf people marrying other deaf people, would not make much difference. Even if deaf people substantially out-reproduced normals, which they don’t, only ~1-2% of the copies of 35delG reside in deaf people.
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may 2017 by nhaliday
Solidarity Forever | West Hunter
If you had a gene with a conspicuous effect (like a green beard) that at the same time caused the carrier to favor other individuals with a green beard, you could get a very powerful kind of genetic altruism, one not limited to close relatives. A very strong effect, one that caused you to act as if other carriers were just as valuable as you are (as if other carriers were your identical twin) could exist, but weaker effects (green fuzz) could also be favored by selection – if you were just somewhat more likely to cooperate with others bearing the mark. That could be enough to drive strong selection for the gene, and might not even be terribly noticeable.

This might be especially powerful in humans: we have so very many ways of cooperating or tripping each other up. Now and then you get partial alignment of interests, and remarkable things happen. If we could all just get along, we could conquer the world and make everyone else our slaves and playthings!

...

Shortly after the Green Beards became influential, you’d see a lot of people wearing fake green beards, which would cut down on the advantage and possibly turn green beards into easy marks, chumps doomed to failure. It would work best if the identifying mark was hard to copy – difficult today, but in the past some things, eye color for example, would have been hard to copy.

This all gets complicated, since it’s not always easy to know what someone else’s best interest is – let along that of the entire Greenbeard race. For that matter it’s not always that easy to know what your own best interest is.

I’m for it, of course: trying to fighting off such a mutant takeover would make life more interesting.

https://westhunt.wordpress.com/2015/03/11/solidarity-forever/#comment-67414
There no evidence, that I know of, of anything like a strong green-beard effect in humans. If there was one, it would have dramatic consequences, which we haven’t observed, so I doubt if one exists. Although we could always create one, for laughs.

Any gene that selected for extended kin altruism would not flourish – would not increase in frequency – because the expensive altruistic effort would not be focused on people who were more likely than average (in that population!) to carry the relevant allele. Which means that every time that expensive altruism happened, the average allele frequency in that population would go down, not up: this is not the route to success. If you can’t understand, that’s your problem.

Frank Salter is entirely wrong. There is no such thing as “genetic interest”, in the sense he’s talking about, not one that makes people feel the way he’d like them to. Sheesh, if there were, he wouldn’t have to argue about it, anymore than you have to argue parents into caring about their children. Now if he said that having more Swedes in the world would result in something he liked, that could well be true: but there’s no instinct that says everyone, even most Swedes, have to favor that course.

You have to do the math: when you do, this idea doesn’t work. And that’s the end of this conversation.

https://westhunt.wordpress.com/2015/03/11/solidarity-forever/#comment-67424
That lady’s mind ain’t right.

Speaking of which, one has to wonder which is the greater threat – the increasing dumb fraction of this country, or the increasing crazy fraction.
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may 2017 by nhaliday
Estimating the number of unseen variants in the human genome
To find all common variants (frequency at least 1%) the number of individuals that need to be sequenced is small (∼350) and does not differ much among the different populations; our data show that, subject to sequence accuracy, the 1000 Genomes Project is likely to find most of these common variants and a high proportion of the rarer ones (frequency between 0.1 and 1%). The data reveal a rule of diminishing returns: a small number of individuals (∼150) is sufficient to identify 80% of variants with a frequency of at least 0.1%, while a much larger number (> 3,000 individuals) is necessary to find all of those variants.

A map of human genome variation from population-scale sequencing: http://www.internationalgenome.org/sites/1000genomes.org/files/docs/nature09534.pdf

Scientists using data from the 1000 Genomes Project, which sequenced one thousand individuals from 26 human populations, found that "a typical [individual] genome differs from the reference human genome at 4.1 million to 5.0 million sites … affecting 20 million bases of sequence."[11] Nearly all (>99.9%) of these sites are small differences, either single nucleotide polymorphisms or brief insertion-deletions in the genetic sequence, but structural variations account for a greater number of base-pairs than the SNPs and indels.[11]

Human genetic variation: https://en.wikipedia.org/wiki/Human_genetic_variation

Singleton Variants Dominate the Genetic Architecture of Human Gene Expression: https://www.biorxiv.org/content/early/2017/12/15/219238
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may 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.
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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.
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may 2017 by nhaliday
Typos | West Hunter
In a simple model, a given mutant has an equilibrium frequency μ/s, when μ is the mutation rate from good to bad alleles and s is the size of the selective disadvantage. To estimate the total impact of mutation at that locus, you multiply the frequency by the expected harm, s: which means that the fitness decrease (from effects at that locus) is just μ, the mutation rate. If we assume that these fitness effects are multiplicative, the total fitness decrease (also called ‘mutational load’) is approximately 1 – exp(-U), when U is where U=Σ2μ, the total number of new harmful mutations per diploid individual.

https://westhunt.wordpress.com/2012/10/17/more-to-go-wrong/

https://westhunt.wordpress.com/2012/07/13/sanctuary/
interesting, suggestive comment on Africa:
https://westhunt.wordpress.com/2012/07/13/sanctuary/#comment-3671
https://westhunt.wordpress.com/2012/07/14/too-darn-hot/
http://infoproc.blogspot.com/2012/07/rare-variants-and-human-genetic.html
https://westhunt.wordpress.com/2012/07/18/changes-in-attitudes/
https://westhunt.wordpress.com/2012/08/24/men-and-macaques/
I have reason to believe that few people understand genetic load very well, probably for self-referential reasons, but better explanations are possible.

One key point is that the amount of neutral variation is determined by the long-term mutational rate and population history, while the amount of deleterious variation [genetic load] is set by the selective pressures and the prevailing mutation rate over a much shorter time scale. For example, if you consider the class of mutations that reduce fitness by 1%, what matters is the past few thousand years, not the past few tens or hundreds of of thousands of years.

...

So, assuming that African populations have more neutral variation than non-African populations (which is well-established), what do we expect to see when we compare the levels of probably-damaging mutations in those two populations? If the Africans and non-Africans had experienced essentially similar mutation rates and selective pressures over the past few thousand years, we would expect to see the same levels of probably-damaging mutations. Bottlenecks that happened at the last glacial maximum or in the expansion out of Africa are irrelevant – too long ago to matter.

But we don’t. The amount of rare synonymous stuff is about 22% higher in Africans. The amount of rare nonsynonymous stuff (usually at least slightly deleterious) is 20.6% higher. The number of rare variants predicted to be more deleterious is ~21.6% higher. The amount of stuff predicted to be even more deleterious is ~27% higher. The number of harmful looking loss-of-function mutations (yet more deleterious) is 25% higher.

It looks as if the excess grows as the severity of the mutations increases. There is a scenario in which this is possible: the mutation rate in Africa has increased recently. Not yesterday, but, say, over the past few thousand years.

...

What is the most likely cause of such variations in the mutation rate? Right now, I’d say differences in average paternal age. We know that modest differences (~5 years) in average paternal age can easily generate ~20% differences in the mutation rate. Such between-population differences in mutation rates seem quite plausible, particularly since the Neolithic.
https://westhunt.wordpress.com/2016/04/10/bugs-versus-drift/
more recent: https://westhunt.wordpress.com/2017/06/06/happy-families-are-all-alike-every-unhappy-family-is-unhappy-in-its-own-way/#comment-92491
Probably not, but the question is complex: depends on the shape of the deleterious mutational spectrum [which we don’t know], ancient and recent demography, paternal age, and the extent of truncation selection in the population.
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may 2017 by nhaliday
The Issue that Time Forgot | West Hunter
Human population genetics in the 1960s was obsessed with the question of genetic load. Much of the motivation was concern about health consequences of radiation and nuclear weapons. We now know that radiation does bad things to organisms but that the mutation rate in mammals is nearly insensitive to the effects of ionizing radiation. No one knew that then. Popular concern about the issue was also pumped up by monster movies, which were everywhere on late night television. Does anyone remember Godzilla?

...

The key paper about load was published in 19582. Morton, Crow, and Muller showed that, under some simplifying assumptions, the regression of mortality (and on other traits like IQ) on the inbreeding coefficient could reveal the nature of our burden of mutations. In particular the negative logarithm of the rate, for example the infant mortality rate, should be linear in the inbreeding coefficient:

-ln(q) = A + Bf

where q is the mortality rate and f the inbreeding coefficient. Their important insight was the if our load is mostly deleterious recessives then the rate should increase rapidly with inbreeding. If, on the other hand, our load reflects a lot of balanced polymorphisms then the load should not increase very much with inbreeding. In particular the load ratio, B/A, ought to be something like 10 if there are a lot of deleterious recessives while something like 2 if there are a lot of balanced polymorphisms. A clear explanation of the the theory and the results availabe by the early 1970s can be found in the classic Cavalli and Bodmer text3.

The bottom line was that load ratios from human populations did not give a clear signal either way. A typical B/A ratio was something like 4. The interest in and optimism about load theory in 1960 had fizzled by 1970.

Today all those issues are back on the table in a big way. What is our burden of mutation? How many of our aches and pains and premature deaths are costs of balanced polymorphism? Unfortunately the whole toolkit of 50 years ago has been mostly forgotten by the current generation of human population geneticists. A shame.

- Harpending
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april 2017 by nhaliday
Polygyny, Fertility, and Savings
For reasonable parameter values, I find that banning polygyny decreases fertility by 40 percent, increases savings by 70 percent, and increases output per capita by 170 percent.

also interesting:
Table A1 shows that almost all men do marry by age 50 in these countries. Thus the common perception that two wives for some men means no wives for equally many men is wrong. Since the sex ratios in most countries do not deviate much from one, one may wonder how such a high incidence of polygyny is possible. The answer to this puzzle lies in extremely high spousal age gaps coupled with high population growth (Tertilt 2004).7 Table 1 shows that the average age gap at first marriage is almost seven years in highly polygynous countries. Annual population growth in this area is 2.7 percent, which amounts to a 20 percent increase in cohort size over seven years. On average, each man could therefore marry 1.2 wives, or, put differently, 20 percent of the population could marry two wives.8

AFRICAN POLYGAMY: PAST AND PRESENT: http://voxeu.org/article/african-polygamy-past-and-present
https://www.dartmouth.edu/~neudc2012/docs/paper_3.pdf
https://twitter.com/FinchesofDarwin/status/903319029732884481
http://voxeu.org/article/understanding-long-run-effects-africa-s-slave-trades
This has led the authors to conclude that Africa’s history of the slave trades is the primary explanation for why today polygyny is much more prevalent in West Africa than in East Africa.
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april 2017 by nhaliday
How America made Scandinavian social democracy possible | FT Alphaville
The methodology centres on names. Psychologists have long found that people with relatively rare names are more likely to be “unique”, presumably because parents who consciously choose rare names for their children would be more likely to raise them to be nonconformists.

The researchers have access to all the names of people who lived in Norway and Sweden throughout the great migration wave, as well as all the names of the people who left for America. They also have the same information broken down by locality for a more fine-grained analysis.

They found that while “individualism” rose modestly overall, the places with more emigration became relatively more “collectivist” than those regions with less emigraton.

https://ehsthelongrun.net/2017/06/13/the-making-of-new-world-individualism-and-old-world-collectivism-international-migrants-as-carriers-of-cultural-values/
https://twitter.com/pseudoerasmus/status/847789231296610308

more on this by Gwern: https://www.gwern.net/Statistical-notes#selective-emigration-and-personality-trait-change
Knudsen 2019 finds that the emigration of 25% of the Scandinavian population to the USA 1850–1920 was driven in part by more ‘individualistic’ personality factors among emigrants, leading to permanent decreases in mean ‘individualism’ in the home countries. This is attributed to cultural factors, rather than genetics. I model the overall migration as a simple truncation selection scenario, and find that in a simple model under reasonable assumptions, the entire effect could be genetic.
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march 2017 by nhaliday
Interview Greg Cochran by Future Strategist
https://westhunt.wordpress.com/2016/08/10/interview/

- IQ enhancement (somewhat apprehensive, wonder why?)
- ~20 years to CRISPR enhancement (very ballpark)
- cloning as an alternative strategy
- environmental effects on IQ, what matters (iodine, getting hit in the head), what doesn't (schools, etc.), and toss-ups (childhood/embryonic near-starvation, disease besides direct CNS-affecting ones [!])
- malnutrition did cause more schizophrenia in Netherlands (WW2) and China (Great Leap Forward) though
- story about New Mexico schools and his children (mostly grad students in physics now)
- clever sillies, weird geniuses, and clueless elites
- life-extension and accidents, half-life ~ a few hundred years for a typical American
- Pinker on Harvard faculty adoptions (always Chinese girls)
- parabiosis, organ harvesting
- Chicago economics talk
- Catholic Church, cousin marriage, and the rise of the West
- Gregory Clark and Farewell to Alms
- retinoblastoma cancer, mutational load, and how to deal w/ it ("something will turn up")
- Tularemia and Stalingrad (ex-Soviet scientist literally mentioned his father doing it)
- germ warfare, nuclear weapons, and testing each
- poison gas, Haber, nerve gas, terrorists, Japan, Syria, and Turkey
- nukes at https://en.wikipedia.org/wiki/Incirlik_Air_Base
- IQ of ancient Greeks
- history of China and the Mongols, cloning Genghis Khan
- Alexander the Great vs. Napoleon, Russian army being late for meetup w/ Austrians
- the reason why to go into Iraq: to find and clone Genghis Khan!
- efficacy of torture
- monogamy, polygamy, and infidelity, the Aboriginal system (reverse aging wives)
- education and twin studies
- errors: passing white, female infanticide, interdisciplinary social science/economic imperialism, the slavery and salt story
- Jewish optimism about environmental interventions, Rabbi didn't want people to know, Israelis don't want people to know about group differences between Ashkenazim and other groups in Israel
- NASA spewing crap on extraterrestrial life (eg, thermodynamic gradient too weak for life in oceans of ice moons)
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march 2017 by nhaliday
Kin selection - Wikipedia
Formally, genes should increase in frequency when

{\displaystyle rB>C}
where

r=the genetic relatedness of the recipient to the actor, often defined as the probability that a gene picked randomly from each at the same locus is identical by descent.
B=the additional reproductive benefit gained by the recipient of the altruistic act,
C=the reproductive cost to the individual performing the act.
This inequality is known as Hamilton's rule after W. D. Hamilton who in 1964 published the first formal quantitative treatment of kin selection.

The relatedness parameter (r) in Hamilton's rule was introduced in 1922 by Sewall Wright as a coefficient of relationship that gives the probability that at a random locus, the alleles there will be identical by descent.[20] Subsequent authors, including Hamilton, sometimes reformulate this with a regression, which, unlike probabilities, can be negative. A regression analysis producing statistically significant negative relationships indicates that two individuals are less genetically alike than two random ones (Hamilton 1970, Nature & Grafen 1985 Oxford Surveys in Evolutionary Biology). This has been invoked to explain the evolution of spiteful behaviour consisting of acts that result in harm, or loss of fitness, to both the actor and the recipient.

Several scientific studies have found that the kin selection model can be applied to nature. For example, in 2010 researchers used a wild population of red squirrels in Yukon, Canada to study kin selection in nature. The researchers found that surrogate mothers would adopt related orphaned squirrel pups but not unrelated orphans. The researchers calculated the cost of adoption by measuring a decrease in the survival probability of the entire litter after increasing the litter by one pup, while benefit was measured as the increased chance of survival of the orphan. The degree of relatedness of the orphan and surrogate mother for adoption to occur depended on the number of pups the surrogate mother already had in her nest, as this affected the cost of adoption. The study showed that females always adopted orphans when rB > C, but never adopted when rB < C, providing strong support for Hamilton's rule.[21]
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march 2017 by nhaliday
There is no fitness but fitness, and the lineage is its bearer | Philosophical Transactions of the Royal Society B: Biological Sciences
We argue that this understanding of inclusive fitness based on gene lineages provides the most illuminating and accurate picture and avoids pitfalls in interpretation and empirical applications of inclusive fitness theory.
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march 2017 by nhaliday
Eebers and robbers | West Hunter
A year or so ago I was on a review committee for a department of biology. It was a pleasant and productive department, but it soon became apparent to us that it was in effect two departments sharing the same building. One was eeb (ecology and evolutionary biology), while the other was, in their jargon, rob (the rest of biology.) Relations were cordial between the two for the most part but there was almost no interaction nor interest across the divide.

The same divide is increasingly apparent in genetics, genomics, and human evolution. Several years ago a colleague suggested to me that the idea that mathematics is the language of science was no longer very accurate. There are, he said, two languages of science, one being mathematics and other organic chemistry. He was onto something. People who speak mathematics and models, eebers, and people who speak organic chemistry, robbers, are more and more out of touch with each other.
west-hunter  science  academia  tribalism  lens  things  bio  evolution  genetics  population-genetics  big-picture  reflection  scitariat 
march 2017 by nhaliday
Minor allele frequency - Wikipedia
It is widely used in population genetics studies because it provides information to differentiate between common and rare variants in the population.
jargon  genetics  genomics  bioinformatics  population-genetics  QTL  wiki  reference  metrics  distribution 
march 2017 by nhaliday
Religion, fertility and genes: a dual inheritance model | Proceedings of the Royal Society of London B: Biological Sciences
The paper considers the effect of religious defections and exogamy on the religious and genetic composition of society. Defections reduce the ultimate share of the population with religious allegiance and slow down the spread of the religiosity gene. However, provided the fertility differential persists, and people with a religious allegiance mate mainly with people like themselves, the religiosity gene will eventually predominate despite a high rate of defection. This is an example of ‘cultural hitch-hiking’, whereby a gene spreads because it is able to hitch a ride with a high-fitness cultural practice.
study  org:nat  bio  sapiens  evolution  biodet  genetics  population-genetics  coordination  group-selection  culture  religion  models  🌞  fertility  correlation  simulation  institutions  EGT  dynamical  GT-101  theos  the-bones  ecology 
march 2017 by nhaliday
Evolution Runs Faster on Short Timescales | Quanta Magazine
But if more splashes of paint appear on a wall, they will gradually conceal some of the original color beneath new layers. Similarly, evolution and natural selection write over the initial mutations that appear over short timescales. Over millions of years, an A in the DNA may become a T, but in the intervening time it may be a C or a G for a while. Ho believes that this mutational saturation is a major cause of what he calls the time-dependent rate phenomenon.

“Think of it like the stock market,” he said. Look at the hourly or daily fluctuations of Standard & Poor’s 500 index, and it will appear wildly unstable, swinging this way and that. Zoom out, however, and the market appears much more stable as the daily shifts start to average out. In the same way, the forces of natural selection weed out the less advantageous and more deleterious mutations over time.
news  org:mag  org:sci  evolution  bio  nature  mutation  selection  time  methodology  stylized-facts  genetics  population-genetics  genomics  speed  pigeonhole-markov  bits  nibble  org:inst 
march 2017 by nhaliday
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