nhaliday + sib-study   27

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
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 
april 2019 by nhaliday
Frontiers | Can We Validate the Results of Twin Studies? A Census-Based Study on the Heritability of Educational Achievement | Genetics
As for most phenotypes, the amount of variance in educational achievement explained by SNPs is lower than the amount of additive genetic variance estimated in twin studies. Twin-based estimates may however be biased because of self-selection and differences in cognitive ability between twins and the rest of the population. Here we compare twin registry based estimates with a census-based heritability estimate, sampling from the same Dutch birth cohort population and using the same standardized measure for educational achievement. Including important covariates (i.e., sex, migration status, school denomination, SES, and group size), we analyzed 893,127 scores from primary school children from the years 2008–2014. For genetic inference, we used pedigree information to construct an additive genetic relationship matrix. Corrected for the covariates, this resulted in an estimate of 85%, which is even higher than based on twin studies using the same cohort and same measure. We therefore conclude that the genetic variance not tagged by SNPs is not an artifact of the twin method itself.
study  biodet  behavioral-gen  iq  psychometrics  psychology  cog-psych  twin-study  methodology  variance-components  state-of-art  🌞  developmental  age-generation  missing-heritability  biases  measurement  sampling-bias  sib-study 
december 2017 by nhaliday
Reconsidering the Heritability of Intelligence in Adulthood: Taking Assortative Mating and Cultural Transmission into Account
Heritability estimates of general intelligence in adulthood generally range from 75 to 85%, with all heritability due to additive genetic influences, while genetic dominance and shared environmental factors are absent, or too small to be detected. These estimates are derived from studies based on the classical twin design and are based on the assumption of random mating. Yet, considerable positive assortative mating has been reported for general intelligence. Unmodeled assortative mating may lead to biased estimates of the relative magnitude of genetic and environmental factors.

...

Under the preferred phenotypic assortment model, the variance of intelligence in adulthood was not only due to non-shared environmental (18%) and additive genetic factors (44%) but also to non-additive genetic factors (27%) and phenotypic assortment (11%).This non-additive nature of genetic influences on intelligence needs to be accommodated in future GWAS studies for intelligence.
study  biodet  behavioral-gen  psychology  cog-psych  iq  twin-study  sib-study  biases  gotchas  models  map-territory  assortative-mating  variance-components  🌞  nonlinearity  regularizer  intricacy 
november 2017 by nhaliday
1 Genetics and Crime
The broader construct of antisocial behavior – which includes criminal offending, as well as aggression – also shows substantial genetic influence. In a meta-analysis combining effect sizes in 51 twin and adoption studies, Rhee and Waldman (2002) reported a heritability estimate of 41 per cent, with the remaining 59 per cent of variance being due to environmental factors. Interestingly, when comparing results for various definitions of antisocial behavior, only criminal offending appeared to be influenced by both additive genetic effects and non-additive genetic effects – possibly due to genetic dominance and epistatic interactions between genes – based on a pattern of results whereby, on average, identical (monozygotic) twin correlations are more than twice the value of fraternal (dizygotic) twin correlations, and also that biological parent–offspring correlations are less than fraternal twin correlations. Such non-additive genetic effects could arise if one or more high risk alleles act in a recessive fashion, or if certain alleles at one locus affect gene expression at other loci (epistasis).

One intriguing aspect of the literature on genetics and crime is that the strong and consistent genetic influence seen for property offending does not hold true for violent criminal convictions. None of the major adoption studies in Scandinavia or the United States found any elevated risk for violent convictions as a function of either biological or adoptive parent criminal offending, although one early twin study did find greater identical (monozygotic) than fraternal (dizygotic) concordance for violent convictions (see Cloninger and Gottesman, 1987). This pattern of twin, but not parent-offspring, similarity for violent criminal behavior suggests the possibility of non-additive genetic effects due to dominance or epistasis, which would result in increased resemblance for siblings (and twins), but not for parents and offspring. Thus, there may be genetic risk for violent crimes such as murder and rape, which may stem from rare recessive genes, or specific combinations of alleles that do not appear in studies of vertical transmission across generations.

A Swedish national twin study of criminal behavior and its violent, white-collar and property subtypes: https://www.cambridge.org/core/journals/psychological-medicine/article/a-swedish-national-twin-study-of-criminal-behavior-and-its-violent-white-collar-and-property-subtypes/0D9A88185ED0FD5525A5EBD5D2EBA117
For all criminal convictions, heritability was estimated at around 45% in both sexes, with the shared environment accounting for 18% of the variance in liability in females and 27% in males. The correlation of these risk factors across sexes was estimated at +0.63. In men, the magnitudes of genetic and environmental influence were similar in the three criminal conviction subtypes. However, for violent and white-collar convictions, nearly half and one-third of the genetic effects were respectively unique to that criminal subtype. About half of the familial environmental effects were unique to property convictions.

Heritability, Assortative Mating and Gender Differences in Violent Crime: Results from a Total Population Sample Using Twin, Adoption, and Sibling Models: https://link.springer.com/article/10.1007/s10519-011-9483-0
Using 36k twins, violent crime was moderately heritable (~ 55%) w/ 13% shared environment influence. Using 1.5 mil siblings, heritability was higher for males, & family environment higher for females. Moderate assortative mating for violent crime (r = .4).

The impact of neighbourhood deprivation on adolescent violent criminality and substance misuse: A longitudinal, quasi-experimental study of the total Swedish population: https://academic.oup.com/ije/article/42/4/1057/656274/The-impact-of-neighbourhood-deprivation-on
In the crude model, an increase of 1 SD in neighbourhood deprivation was associated with a 57% increase in the odds of being convicted of a violent crime (95% CI 52%–63%). The effect was greatly attenuated when adjustment was made for a number of observed confounders (OR 1.09, 95% CI 1.06–1.11). When we additionally adjusted for unobserved familial confounders, the effect was no longer present (OR 0.96, 95% CI 0.84–1.10). Similar results were observed for substance misuse. The results were not due to poor variability either between neighbourhoods or within families.

Childhood family income, adolescent violent criminality and substance misuse: quasi-experimental total population study: http://bjp.rcpsych.org/content/early/2014/08/14/bjp.bp.113.136200
https://www.economist.com/news/science-and-technology/21613303-disturbing-study-link-between-incomes-and-criminal-behaviour-have-and
What did surprise him was that when he looked at families which had started poor and got richer, the younger children—those born into relative affluence—were just as likely to misbehave when they were teenagers as their elder siblings had been. Family income was not, per se, the determining factor.

Indicators of domestic/intimate partner violence are structured by genetic and nonshared environmental influences: https://www.researchgate.net/publication/233737219_Indicators_of_domesticintimate_partner_violence_are_structured_by_genetic_and_nonshared_environmental_influences
Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance.
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october 2017 by nhaliday
Why are children in the same family so different from one another? - PubMed - NCBI
- Plomin et al

The article has three goals: (1) To describe quantitative genetic methods and research that lead to the conclusion that nonshared environment is responsible for most environmental variation relevant to psychological development, (2) to discuss specific nonshared environmental influences that have been studied to date, and (3) to consider relationships between nonshared environmental influences and behavioral differences between children in the same family. The reason for presenting this article in BBS is to draw attention to the far-reaching implications of finding that psychologically relevant environmental influences make children in a family different from, not similar to, one another.
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october 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
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
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
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
Epidemiology of autism - Wikipedia
https://spectrumnews.org/news/school-survey-india-reveals-low-autism-prevalence/
This Is How Much of Autism Is Genetic: http://time.com/4956316/how-much-of-autism-is-genetic/
Indeed, when Sandin tracked autism diagnoses over time among the sibling pairs, he found that genetics likely accounts for around 83% of the disorder. That compares to nearly 90% reported in previous studies of twins only. Using the new model, environmental factors probably contribute around 17% to the risk of developing autism.
sapiens  medicine  genetics  variance-components  science-anxiety  psychiatry  disease  neuro  autism  👽  epidemiology  wiki  reference  biodet  paternal-age  behavioral-gen  public-health  multi  news  org:mag  org:sci  india  asia  data  sib-study  study  summary  org:lite 
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
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
Confounder Of The Day: How Sexy Your Parents Were | Slate Star Codex
- "paternal age effect" just a selection effect (men w/ issues end up having kids later due to difficulty finding a mate)
- one other suggested inconsistent explanation: spermatogenic selfish-gene effect
- interesting discussion of sperm freezing
yvain  ssc  psychiatry  medicine  aging  developmental  study  summary  genetic-load  hmm  biodet  causation  planning  parenting  paternal-age  disease  sex  gender  selfish-gene  gwern  confounding  EGT  epidemiology  null-result  sib-study  ratty  behavioral-gen  cooperate-defect  age-generation 
february 2017 by nhaliday
Maternal smoking during pregnancy and adverse outcomes in offspring: genetic and environmental sources of covariance. - PubMed - NCBI
The results suggest that the associations between SDP in mothers and cognition and externalizing behaviors in their offspring is primarily due to genetic effects that influence the behaviors in both generations.

low birth weight though
study  health  developmental  disease  neuro  variance-components  europe  nordic  sib-study  biodet 
january 2017 by nhaliday
The Genetic Correlation between Height and IQ: Shared Genes or Assortative Mating?
Both traits were highly heritable, although there was greater evidence for non-additive genetic effects in males. After accounting for assortative mating, the correlation between height and IQ was found to be almost entirely genetic in nature. Model fits indicate that both pleiotropy and assortative mating contribute significantly and about equally to this genetic correlation.
study  embodied  iq  genetic-correlation  assortative-mating  twin-study  sib-study  correlation  biodet  science-anxiety  behavioral-gen 
november 2016 by nhaliday
Divorce and children’s long-term outcomes | VOX, CEPR’s Policy Portal
It has been widely demonstrated that parental divorce is associated with negative outcomes for affected children. However, the degree of causality in this relationship is not as clear. This column tackles this problem by using the level of gender integration in fathers’ workplaces as an instrument for divorce. The results suggest a causal link between divorce and worse economic outcomes that persists into early adulthood.
http://ftp.iza.org/dp9928.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904543/
The literature on father absence is frequently criticized for its use of cross-sectional data and methods that fail to take account of possible omitted variable bias and reverse causality. We review studies that have responded to this critique by employing a variety of innovative research designs to identify the causal effect of father absence, including studies using lagged dependent variable models, growth curve models, individual fixed effects models, sibling fixed effects models, natural experiments, and propensity score matching models. Our assessment is that studies using more rigorous designs continue to find negative effects of father absence on offspring well-being, although the magnitude of these effects is smaller than what is found using traditional cross-sectional designs. The evidence is strongest and most consistent for outcomes such as high school graduation, children’s social-emotional adjustment, and adult mental health.

Genetics, the Rearing Environment, and the Intergenerational Transmission of Divorce: A Swedish National Adoption Study: http://journals.sagepub.com/doi/abs/10.1177/0956797617734864
There was stronger resemblance to lived-with mothers, providing indirect evidence of rearing-environment influences on the intergenerational transmission of divorce. The heritability of divorce assessed across generations was 0.13. We attempted to replicate our findings using within-generation data from adoptive and biological siblings (ns = 8,523–53,097). Adoptees resembled their biological, not adoptive, siblings in their history of divorce. Thus, there was consistent evidence that genetic factors contributed to the intergenerational transmission of divorce but weaker evidence for a rearing-environment effect of divorce. Within-generation data from siblings supported these conclusions.

The Long-Term Effects of Legalizing Divorce on Children: http://onlinelibrary.wiley.com/doi/10.1111/obes.12200/abstract
We find that women who grew up under legal divorce have lower earnings and income and worse health as adults compared with women who grew up under illegal divorce. These negative effects are not found for men.

Father Absence and Reproductive Strategy: An Evolutionary Perspective: http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1037&context=anthropologyfacpub
interesting fact: father-absent childhood raises verbal and lowers math/spatial aptitude

Relation of Type and Onset of Father Absence to Cognitive Development: http://sci-hub.tw/http://www.jstor.org/stable/1127548
gender  causation  study  parenting  regularizer  long-term  developmental  environmental-effects  biodet  natural-experiment  confounding  sociology  org:ngo  intervention  endo-exo  multi  pdf  gender-diff  article  life-history  white-paper  meta-analysis  survey  education  labor  stress  psychiatry  dignity  endogenous-exogenous  sib-study  behavioral-gen  europe  nordic  psychology  social-psych  roots  variance-components  genetics  science-anxiety  chart  branches  cost-benefit  institutions  social-structure  health  demographics  compensation  policy  law  control  west-hunter  scitariat  anthropology  evopsych  sex  sexuality  rot  coming-apart  social-norms  stylized-facts  correlation  🌞  tradeoffs  class  sapiens  speculation  iq  language  spatial  psych-architecture  history  mostly-modern  data  comparison  personality  things  world-war  direction  cultural-dynamics  usa  higher-ed  harvard  phalanges  piracy  gnosis-logos  dirty-hands  embodied  the-world-is-just-atoms  cog-psych  intelligence  begin-mid 
august 2016 by nhaliday

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