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An adaptability limit to climate change due to heat stress
Despite the uncertainty in future climate-change impacts, it is often assumed that humans would be able to adapt to any possible warming. Here we argue that heat stress imposes a robust upper limit to such adaptation. Peak heat stress, quantified by the wet-bulb temperature TW, is surprisingly similar across diverse climates today. TW never exceeds 31 °C. Any exceedence of 35 °C for extended periods should induce hyperthermia in humans and other mammals, as dissipation of metabolic heat becomes impossible. While this never happens now, it would begin to occur with global-mean warming of about 7 °C, calling the habitability of some regions into question. With 11–12 °C warming, such regions would spread to encompass the majority of the human population as currently distributed. Eventual warmings of 12 °C are possible from fossil fuel burning. One implication is that recent estimates of the costs of unmitigated climate change are too low unless the range of possible warming can somehow be narrowed. Heat stress also may help explain trends in the mammalian fossil record.

Trajectories of the Earth System in the Anthropocene: http://www.pnas.org/content/early/2018/07/31/1810141115
We explore the risk that self-reinforcing feedbacks could push the Earth System toward a planetary threshold that, if crossed, could prevent stabilization of the climate at intermediate temperature rises and cause continued warming on a “Hothouse Earth” pathway even as human emissions are reduced. Crossing the threshold would lead to a much higher global average temperature than any interglacial in the past 1.2 million years and to sea levels significantly higher than at any time in the Holocene. We examine the evidence that such a threshold might exist and where it might be.
study  org:nat  environment  climate-change  humanity  existence  risk  futurism  estimate  physics  thermo  prediction  temperature  nature  walls  civilization  flexibility  rigidity  embodied  multi  manifolds  plots  equilibrium  phase-transition  oscillation  comparison  complex-systems  earth 
august 2018 by nhaliday
Cultural variation in cultural evolution | Proceedings of the Royal Society of London B: Biological Sciences
Cultural evolutionary models have identified a range of conditions under which social learning (copying others) is predicted to be adaptive relative to asocial learning (learning on one's own), particularly in humans where socially learned information can accumulate over successive generations. However, cultural evolution and behavioural economics experiments have consistently shown apparently maladaptive under-utilization of social information in Western populations. Here we provide experimental evidence of cultural variation in people's use of social learning, potentially explaining this mismatch. People in mainland China showed significantly more social learning than British people in an artefact-design task designed to assess the adaptiveness of social information use. People in Hong Kong, and Chinese immigrants in the UK, resembled British people in their social information use, suggesting a recent shift in these groups from social to asocial learning due to exposure to Western culture. Finally, Chinese mainland participants responded less than other participants to increased environmental change within the task. Our results suggest that learning strategies in humans are culturally variable and not genetically fixed, necessitating the study of the ‘social learning of social learning strategies' whereby the dynamics of cultural evolution are responsive to social processes, such as migration, education and globalization.

...

Western education emphasizes individual discovery and creativity, whereas East Asian education emphasizes rote learning from authority [25]. The adoption of consumer products shows less social influence in Western than East Asian countries [26]. Westerners are described as more individualistic/independent, while East Asians are described as more collectivistic/interdependent [27], dimensions which intuitively map on to asocial and social learning, respectively.

Societal background influences social learning in cooperative decision making: https://www.sciencedirect.com/science/article/pii/S1090513817303501
We demonstrate that Chinese participants base their cooperation decisions on information about their peers much more frequently than their British counterparts. Moreover, our results reveal remarkable societal differences in the type of peer information people consider. In contrast to the consensus view, Chinese participants tend to be substantially less majority-oriented than the British. While Chinese participants are inclined to adopt peer behavior that leads to higher payoffs, British participants tend to cooperate only if sufficiently many peers do so too. These results indicate that the basic processes underlying social transmission are not universal; rather, they vary with cultural conditions. As success-based learning is associated with selfish behavior and majority-based learning can help foster cooperation, our study suggests that in different societies social learning can play diverging roles in the emergence and maintenance of cooperation.
study  org:nat  anthropology  cultural-dynamics  sapiens  pop-diff  comparison  sociality  learning  duplication  individualism-collectivism  n-factor  europe  the-great-west-whale  china  asia  sinosphere  britain  anglosphere  strategy  environmental-effects  biodet  within-without  auto-learning  tribalism  things  broad-econ  psychology  cog-psych  social-psych  🎩  🌞  microfoundations  egalitarianism-hierarchy  innovation  creative  explanans  education  culture  curiosity  multi  occident  cooperate-defect  coordination  organizing  self-interest  altruism  patho-altruism  orient  ecology  axelrod 
may 2018 by nhaliday
High male sexual investment as a driver of extinction in fossil ostracods | Nature
Sexual selection favours traits that confer advantages in the competition for mates. In many cases, such traits are costly to produce and maintain, because the costs help to enforce the honesty of these signals and cues1. Some evolutionary models predict that sexual selection also produces costs at the population level, which could limit the ability of populations to adapt to changing conditions and thus increase the risk of extinction2,3,4.
study  org:nat  bio  evolution  selection  sex  competition  cost-benefit  unintended-consequences  signaling  existence  gender  gender-diff  empirical  branches  rot  modernity  fertility  intervention  explanans  humility  status  matching  ranking  ratty  hanson 
april 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
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.
nibble  pdf  slides  talks  bio  biodet  genetics  genomics  GWAS  genetic-correlation  correlation  methodology  bioinformatics  concept  levers  🌞  tutorial  explanation  pop-structure  gene-drift  ideas  multi  study  org:nat  article  repo  software  tools  libraries  stats  hypothesis-testing  biases  confounding  gotchas  QTL  simulation  survey  preprint  population-genetics 
november 2017 by nhaliday
What Does a “Normal” Human Genome Look Like? | Science
So, what have our first glimpses of variation in the genomes of generally healthy people taught us? First, balancing selection, the evolutionary process that favors genetic diversification rather than the fixation of a single “best” variant, appears to play a minor role outside the immune system. Local adaptation, which accounts for variation in traits such as pigmentation, dietary specialization, and susceptibility to particular pathogens is also a second-tier player. What is on the top tier? Increasingly, the answer appears to be mutations that are “deleterious” by biochemical or standard evolutionary criteria. These mutations, as has long been appreciated, overwhelmingly make up the most abundant form of nonneutral variation in all genomes. A model for human genetic individuality is emerging in which there actually is a “wild-type” human genome—one in which most genes exist in an evolutionarily optimized form. There just are no “wild-type” humans: We each fall short of this Platonic ideal in our own distinctive ways.
article  essay  org:nat  🌞  bio  biodet  genetics  genomics  mutation  genetic-load  QTL  evolution  sapiens  survey  summary  coding-theory  enhancement  signal-noise  egalitarianism-hierarchy  selection  tradeoffs  immune  recent-selection  perturbation  nibble  ideas  forms-instances 
november 2017 by nhaliday
Measles and immunological amnesia | West Hunter
A new paper in Science , by Michael Mina et al,  strongly suggests that measles messes up your immunological defenses for two or three years. This is the likely explanation for the fact that measles inoculation causes much greater decreases in child morbidity and mortality than you’d expect from preventing the deaths directly due to measles infection. The thought is that measles whacks the cells that carry immunological memory, leaving the kid ripe for reinfections.  I think there can be a similar effect with anti-cancer chemotherapy.

If correct, this means that measles is much nastier than previously thought. It must have played a significant role in the demographic collapse of long-isolated peoples (such as the Amerindians). Its advent may have played a role in the population decrease associated with the decline of the Classical world.  Even though it is relatively new (having split off from rinderpest a couple of thousand years ago) strong selection for resistance may have  favored some fairly expensive genetic defenses (something like sickle-cell) in Eurasian populations.

We already know of quite a few complex side effects of infectious disease, such the different kind of immunosuppression we see with AIDs, Burkitt’s lymphoma hitting kids with severe Epstein-Barr infections followed by malaria, acute dengue fever that requires a previous infection by a different strain of dengue, etc: there may well be other important interactions and side effects, news of which has not yet come to Harvard.
west-hunter  scitariat  discussion  ideas  commentary  study  summary  org:nat  epidemiology  bio  health  immune  disease  parasites-microbiome  unintended-consequences  cancer  medicine  long-short-run  usa  farmers-and-foragers  age-of-discovery  speculation  nihil  history  iron-age  mediterranean  the-classics  demographics  population  gibbon  rot  harvard  elite  low-hanging  info-dynamics  being-right  heterodox 
october 2017 by nhaliday
Genome Editing
This collection of articles from the Nature Research journals provides an overview of current progress in developing targeted genome editing technologies. A selection of protocols for using and adapting these tools in your own lab is also included.
news  org:sci  org:nat  list  links  aggregator  chart  info-foraging  frontier  technology  CRISPR  biotech  🌞  survey  state-of-art  article  study  genetics  genomics  speedometer 
october 2017 by nhaliday

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