nhaliday + epigenetics   17

WHO | Priority environment and health risks
also: http://www.who.int/heli/risks/vectors/vector/en/

Environmental factors are a root cause of a significant disease burden, particularly in developing countries. An estimated 25% of death and disease globally, and nearly 35% in regions such as sub-Saharan Africa, is linked to environmental hazards. Some key areas of risk include the following:

- Unsafe water, poor sanitation and hygiene kill an estimated 1.7 million people annually, particularly as a result of diarrhoeal disease.
- Indoor smoke from solid fuels kills an estimated 1.6 million people annually due to respiratory diseases.
- Malaria kills over 1.2 million people annually, mostly African children under the age of five. Poorly designed irrigation and water systems, inadequate housing, poor waste disposal and water storage, deforestation and loss of biodiversity, all may be contributing factors to the most common vector-borne diseases including malaria, dengue and leishmaniasis.
- Urban air pollution generated by vehicles, industries and energy production kills approximately 800 000 people annually.
- Unintentional acute poisonings kill 355 000 people globally each year. In developing countries, where two-thirds of these deaths occur, such poisonings are associated strongly with excessive exposure to, and inappropriate use of, toxic chemicals and pesticides present in occupational and/or domestic environments.
- Climate change impacts including more extreme weather events, changed patterns of disease and effects on agricultural production, are estimated to cause over 150 000 deaths annually.

ed.:
Note the high point at human origin (Africa, Middle East) and Asia. Low points in New World and Europe/Russia. Probably key factor in explaining human psychological variation (Haidt axes, individualism-collectivism, kinship structure, etc.). E.g., compare Islam/Judaism (circumcision, food preparation/hygiene rules) and Christianity (orthodoxy more than orthopraxy, no arbitrary practices for group-marking).

I wonder if the dietary and hygiene laws of Christianity get up-regulated in higher parasite load places (the US South, Middle Eastern Christianity, etc.)?

Also the reason for this variation probably basically boils down how long local microbes have had time to adapt to the human immune system.

obv. correlation: https://pinboard.in/u:nhaliday/b:074ecdf30c50

Tropical disease: https://en.wikipedia.org/wiki/Tropical_disease
Tropical diseases are diseases that are prevalent in or unique to tropical and subtropical regions.[1] The diseases are less prevalent in temperate climates, due in part to the occurrence of a cold season, which controls the insect population by forcing hibernation. However, many were present in northern Europe and northern America in the 17th and 18th centuries before modern understanding of disease causation. The initial impetus for tropical medicine was to protect the health of colonialists, notably in India under the British Raj.[2] Insects such as mosquitoes and flies are by far the most common disease carrier, or vector. These insects may carry a parasite, bacterium or virus that is infectious to humans and animals. Most often disease is transmitted by an insect "bite", which causes transmission of the infectious agent through subcutaneous blood exchange. Vaccines are not available for most of the diseases listed here, and many do not have cures.

cf. Galton: https://pinboard.in/u:nhaliday/b:f72f8e03e729
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july 2018 by nhaliday
Sacred text as cultural genome: an inheritance mechanism and method for studying cultural evolution: Religion, Brain & Behavior: Vol 7, No 3
Yasha M. Hartberg & David Sloan Wilson

Any process of evolution requires a mechanism of inheritance for the transmission of information across generations and the expression of phenotypes during each generation. Genetic inheritance mechanisms have been studied for over a century but mechanisms of inheritance for human cultural evolution are far less well understood. Sacred religious texts have the properties required for an inheritance system. They are replicated across generations with high fidelity and are transcribed into action every generation by the invocation and interpretation of selected passages. In this article we borrow concepts and methods from genetics and epigenetics to study the “expressed phenotypes” of six Christian churches that differ along a conservative–progressive axis. Their phenotypic differences, despite drawing upon the same sacred text, can be explained in part by differential expression of the sacred text. Since the invocation and interpretation of sacred texts are often well preserved, our methods allow the expressed phenotypes of religious groups to be studied at any time and place in history.
study  interdisciplinary  bio  sociology  cultural-dynamics  anthropology  religion  christianity  theos  protestant-catholic  politics  ideology  correlation  organizing  institutions  analogy  genetics  genomics  epigenetics  comparison  culture  pdf  piracy  density  flexibility  noble-lie  deep-materialism  new-religion  universalism-particularism  homo-hetero  hypocrisy  group-selection  models  coordination  info-dynamics  evolution  impact  left-wing  right-wing  time  tradition  spreading  sanctity-degradation  coalitions  trees  usa  social-capital  hari-seldon  wisdom  the-basilisk  frequency  sociality  ecology  analytical-holistic 
january 2018 by nhaliday
Scanners Live in Vain | West Hunter
Of course, finding that the pattern already exists at the age of one month seriously weakens any idea that being poor shrinks the brain: most of the environmental effects you would consider haven’t even come into play in the first four weeks, when babies drink milk, sleep, and poop. Genetics affecting both parents and their children would make more sense, if the pattern shows up so early (and I’ll bet money that, if real,  it shows up well before one month);  but Martha Farah, and the reporter from Nature, Sara Reardon, ARE TOO FUCKING DUMB to realize this.

https://westhunt.wordpress.com/2015/03/31/scanners-live-in-vain/#comment-93791
Correlation between brain volume and IQ is about 0.4 . Shows up clearly in studies with sufficient power.

“poverty affects prenatal environment a lot.” No it does not. “poverty” in this country means having plenty to eat.

The Great IQ Depression: https://westhunt.wordpress.com/2014/03/07/the-great-iq-depression/
We hear that poverty can sap brainpower, reduce frontal lobe function, induce the fantods, etc. But exactly what do we mean by ‘poverty’? If we’re talking about an absolute, rather than relative, standard of living, most of the world today must be in poverty, as well as almost everyone who lived much before the present. Most Chinese are poorer than the official US poverty level, right? The US had fairly rapid economic growth until the last generation or so, so if you go very far back in time, almost everyone was poor, by modern standards. Even those who were considered rich at the time suffered from zero prenatal care, largely useless medicine, tabletless high schools, and slow Internet connections. They had to ride horses that had lousy acceleration and pooped all over the place.

In particular, if all this poverty-gives-you-emerods stuff is true, scholastic achievement should have collapsed in the Great Depression – and with the miracle of epigenetics, most of us should still be suffering those bad effects.

But somehow none of this seems to have gone through the formality of actually happening.
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august 2017 by nhaliday
history and progressive virtue: moral technology, moral fashion, and ancestor-memorial retro-trauma chic – ideologjammin'
https://twitter.com/avermeule/status/879695593261735936
https://archive.is/3LHAG
https://archive.is/to1Z2
A terrific point. The rapidity with which good liberals suddenly internalize and enforce novel norms is striking in itself, content apart.

The rapid shift in moral norms in our society should worry us. We are being conditioned to adapt rather than to hold to our principles.

https://twitter.com/avermeule/status/882649313762881537
https://archive.is/cpIKA
https://archive.is/B229W
A thread on the psychology of liberalism, which replaces historical memory by a stereotyped darkness of the past, to be eternally overcome

losing a battle to push something new forward is understandable. having something repealed? going BACK? this is quite incomprehensible to us

https://twitter.com/ortoiseortoise/status/897570742979633153
https://archive.is/9hJIv
i think it's instinctual, not conscious.

https://twitter.com/AsfMQ/status/857593530952413184
https://archive.is/hVKSp
Almost everybody today is a Whig: ie think in terms of 'moral progress', 'forwards' vs 'backwards' thinking, 'stuck in the past', and so on

https://twitter.com/ortoiseortoise/status/897880623536381952
https://archive.is/wPJ6t
the slope is "progress". we slide down every single one eventually. just read some history; recent history will do; it will become obvious.

https://www.unz.com/isteve/whats-happening-now/
https://ideologjammin.wordpress.com/2017/08/17/liberal-democracy-and-its-apparent-paradoxes/
The real problem is that America has already ceased to be a tolerant society. It has, instead, become a celebratory one.
http://www.americanthinker.com/blog/2015/07/bruce_jenner_brett_favre_and_the_cultural_totalitarians.html
In a truly surreal display, NFL great Brett Favre is being denounced by the left’s new cultural commissars for not clapping long and hard enough at ESPN’s ESPY awards, as Bruce/“Caitlyn” Jenner received a “Courage” award for his efforts to become a woman. Oddly, Favre did applaud – not doing so would have been a grave heresy to America’s new church of progressive inquisitors. His sin was not applauding enthusiastically enough.

...

In fact, it all smacks of the gulag – literally. On my shelf at my office is Alexander Solzhenitsyn’s classic, The Gulag Archipelago. There, on page 69 of volume 1, is a chilling account of a Stalinist Soviet Union where men were actually penalized for not clapping ardently enough.

Transgenderism Is Propaganda Designed To Humiliate And Compel Submission: https://www.socialmatter.net/2017/09/26/transgenderism-is-propaganda-designed-to-humiliate-and-compel-submission/
- ARTHUR GORDIAN
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june 2017 by nhaliday
Genetically engineered humans will arrive sooner than you think. And we're not ready. - Vox
lol "epigenetics" makes an appearance ofc

https://www.theatlantic.com/science/archive/2017/06/the-moral-question-that-stanfords-bioengineering-students-get/531876/

For now, that’s prohibitively expensive, but it won’t always be that way. In 2003, it cost 4 dollars to press one of the keys on Endy’s hypothetical synthesizer. This month, it costs just two cents—a 200-fold decrease in price in just 14 years. In the same time frame, the cost of tuition at Stanford has doubled, and is now around $50,000. Given all of that, the first question that Stanford’s budding bioengineers get is this:

At what point will the cost of printing DNA to create a human equal the cost of teaching a student in Stanford?
And the answer is: 19 years from today.

But the follow-up question is a little more complicated:

If you and your future partner are planning to have kids, would you start saving money for college tuition, or for printing the genome of your offspring?
The question tends to split students down the line, says Endy. About 60 percent say that printing a genome is wrong, and flies against what it means to be a parent. They prize the special nature of education and would opt to save for the tuition. But around 40 percent of the class will say that the value of education may change in the future, and if genetic technology becomes mature, and allows them to secure advantages for them and their lineage, they might as well do that.

https://www.nytimes.com/2016/05/14/science/synthetic-human-genome.html
http://www.nature.com/news/plan-to-synthesize-human-genome-triggers-mixed-response-1.20028

https://ipscell.com/2017/06/crispr-human-genetic-modification-a-needed-course-correction/
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may 2017 by nhaliday
Missing heritability problem - Wikipedia
The "missing heritability" problem[1][2][3][4][5][6] can be defined as the fact that single genetic variations cannot account for much of the heritability of diseases, behaviors, and other phenotypes. This is a problem that has significant implications for medicine, since a person's susceptibility to disease may depend more on "the combined effect of all the genes in the background than on the disease genes in the foreground", or the role of genes may have been severely overestimated.

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

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

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

...

7. Genetic effects are indeed through common SNPs acting additively, but are highly polygenic: dispersed over hundreds or thousands of variants each of small effect like a fraction of an inch or a fifth of an IQ point and with low prior probability: unexpected enough that a candidate-gene study is unlikely to select the right SNP out of hundreds of thousands of known SNPs, and GWASes up to 2010, with n<20000, would be unable to find hits which reach genome-wide statistical-significance thresholds. Much larger GWAS sample sizes, often n>100k, would be required to find any hits at all, and would steadily increase after that.
This resolution to the missing heritability problem was supported by the introduction of Genome-wide complex trait analysis (GCTA) in 2010, which demonstrated that trait similarity could be predicted by the genetic similarity of unrelated strangers on common SNPs treated additively, and for many traits the SNP heritability was indeed a substantial fraction of the overall heritability. The GCTA results were further buttressed by findings that a small percent of trait variance could be predicted in GWASes without any genome-wide statistically-significant hits by a linear model including all SNPs regardless of p-value; if there were no SNP contribution, this would be unlikely, but it would be what one expected from SNPs whose effects were very imprecisely estimated by a too-small sample. Combined with the upper bound on maximum effect sizes set by the GWASes up to then, this strongly implied that the highly polygenic theory was correct. Examples of complex traits where increasingly large-scale GWASes have yielded the initial hits and then increasing numbers of hits as sample sizes increased from n<20k to n>100k or n>300k include height,[23] intelligence,[24] and schizophrenia.
article  bio  biodet  behavioral-gen  genetics  genomics  GWAS  candidate-gene  methodology  QTL  missing-heritability  twin-study  measurement  epigenetics  nonlinearity  error  history  mostly-modern  reflection  wiki  reference  science  bounded-cognition  replication  being-right  info-dynamics  🌞  linearity  ideas  GCTA  spearhead 
may 2017 by nhaliday
Intrafamily and intragenomic conflicts in human warfare | Proceedings of the Royal Society of London B: Biological Sciences
We develop a mathematical model to investigate the interplay between sex-specific demography and human warfare, showing that: the ecology of warfare drives the evolution of sex-biased dispersal; sex-biased dispersal modulates intrafamily and intragenomic conflicts in relation to warfare; intragenomic conflict drives parent-of-origin-specific patterns of gene expression—i.e. ‘genomic imprinting’—in relation to warfare phenotypes; and an ecological perspective of conflicts at the levels of the gene, individual, and social group yields novel predictions as to pathologies associated with mutations and epimutations at loci underpinning human violence.

...

A remarkable feature of the kinship theory of genomic imprinting is that it not only illuminates adaptation but also yields testable predictions as to the particular maladaptive phenotypes associated with deleterious genetic and epigenetic mutations [29,30,32,62,75–77]. We have shown that mutations and epimutations tilting the balance towards paternally expressed belligerence and bravery loci are expected to result in ‘aggressive’ and ‘reckless’ pathologies, while those tilting the balance towards maternally expressed loci are expected to result in ‘submissive’ and ‘cowardly’ pathologies, these being extreme phenotypes that lie far beyond the inclusive-fitness optima of any of the individual's genes. Accordingly, our analysis suggests that some instances of societally damaging intergroup violence may represent maladaptive defects rather than well-honed adaptations to our ancestral environment. Understanding that such violence may be associated with imprinting disorders should facilitate discovery of the genes involved.
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march 2017 by nhaliday
An epigenome-wide association study of educational attainment (n = 10,767) | bioRxiv
Two analyses that combine the effects of many probes, polygenic methylation score and epigenetic-clock analyses, both suggest small associations with EA. If our findings regarding EA can be generalized to other biologically distal environmental factors, then they cast doubt on the hypothesis that such factors have large effects on the epigenome.
study  preprint  bio  biodet  genetics  genomics  epigenetics  education 
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."
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march 2017 by nhaliday
Ten Putative Contributors to the Obesity Epidemic
The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects, as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors.
study  meta-analysis  survey  obesity  health  hypochondria  assortative-mating  sleep  model-organism  human-study  🐸  endocrine  metabolic  biodet  epigenetics  epidemiology  sociology  public-health  recent-selection 
january 2017 by nhaliday
Epigenetics | West Hunter
more: https://westhunt.wordpress.com/2015/04/02/back-by-popular-demand/

https://westhunt.wordpress.com/2015/04/02/back-by-popular-demand/#comment-68170
It’s not a real theory, like saying that the wet spot on the kitchen floor is caused by a hole in the roof. All the implications of a real theory are taken seriously (like that hole in the roof will make it cold in the winter). In this kind of pseudo-theory, only the implications that you like exist.

Growing Pains for Field of Epigenetics as Some Call for Overhaul: https://www.nytimes.com/2016/07/02/science/epigenetic-marks-dna-genes.html
https://twitter.com/WiringTheBrain/status/773417464336187392
https://archive.is/RHuF2
For transgenerational epigenetic transmission of behaviour to occur in mammals, here's what would have to happen:

Inherited memories: https://westhunt.wordpress.com/2013/12/13/inherited-memories/
In a recent paper in Nature Neuroscience, Dias and Ressler trained mice to fear the smell of acetophenone. They claim that this reaction was passed on to their offspring, and to the following generation.

I don’t believe a word of it. It would require a mechanism that takes the epigenetic states of genes in the brain, sends that information down to the testes, and then somehow imprints it on the germ cell precursors. And it would have to do this in a very special way, because many epigenetic changes that are the product of learning wouldn’t be the right thing at all during embryogenesis and development: somehow you’d have to pass timing information as well – info that says “methylate this sucker when you’re three weeks old, but not before”. Genes are like a recipe, but this patch would be more like a program. And it’d take a tnuctipun – or better – to prepare it.

According to the blurb at Nature, Kerry Ressler is a neurobiologist and psychiatrist at Emory University. In other words, he’s already a good deal more likely than average to be a flake. He became “interested in epigenetic inheritance after working with poor people living in inner cities, where cycles of drug addiction, neuropsychiatric illness and other problems often seem to recur in parents and their children. So he’s motivated. He’d like this to be true. Too bad.

We’re going to see more and more articles like this: people want to hear it. Tyler Cowen certainly does, but then he may not really be people. None of this research will ever be replicated by anyone careful and honest, but that has hardly stopped a flood of analogous nonsense in the social sciences – for example, how poverty reduces your IQ, unless your name is Abel or Ramanujan.

...

There are more things yet to be discovered than are dreamt of in our philosophy – but there’s even more bullshit. And that’s what this is.
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november 2016 by nhaliday
Epigenetics Has Become Dangerously Fashionable - Facts So Romantic - Nautilus
We’ve witnessed the incursion of epigenetic-hype into our own field of criminology and criminal justice. Recently, we debated scholars in the top criminology journal who argued we should scrap basic behavioral genetics research in no small part because epigenetics was forcing us to “rethink biology” and how genes influence behavior. Reflecting on our debate, we found it ironic that criminology—a field that up until now had been reluctant to discuss genetic influences on behavior—had inexplicably experienced a metamorphosis. Now, epigenetics represented the clear path forward.

On closer inspection, of course, the genesis of this newfound enthusiasm was no mystery. As we mentioned, it resides in the hope that epigenetics heralds the victory of “environmental” over “biological/genetic.” Don’t forget, though, that epigenetics is not a way to hurdle over basic evolutionary principles. Nor does it allow one the luxury of ignoring the rich insights of quantitative genetics and inheritance research. These studies have shown that genetic influences on human outcomes are ubiquitous. Nothing we may learn about transgenerational epigenetics will change that.
bio  genetics  popsci  media  critique  genomics  org:mag  org:sci  biodet  epigenetics 
september 2016 by nhaliday

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