One other observation to make about Sony Pictures’ top-paid executives is that they’re almost entirely white. From some quick Internet searching, fifteen of the seventeen appear to be Caucasian, one (Dwight R. Caines) appears to be African-American, and one (Man Jit Singh) appears to be South Asian. (I’ll update these numbers when and if I hear back from Sony Pictures.) In other words, unless I’m missing something, the upper pay echelon of Sony Pictures is 94 percent male, and 88 percent white. [. . .]To point out the obvious, there's one group overrepresented to a much greater degree than "whites" on this list. By my count, 4 out of 4 of the most highly paid are Jewish, and, looking at the full list, 9 out of the 15 "whites" are known to be Jewish or have distinctively Jewish names (Lynton, Pascal, Mosko, Belgrad, Erlicht, Kaplan, Osher, Weiser, Bersch). In addition, Michael De Luca is half Jewish; based on his physical appearance, Michael Barker is almost certainly Jewish; and I have not investigated the ancestry of the four remaining whites on the list (Clinton Culpepper, Zackary Van Amburg, Tom Bernard, and Michael Pavlic). Jews are overrepresented relative to their share in the US population by at least an order of magnitude. Members of the Northwestern European American majority are massively underrepresented. How does Kevin Roose propose Sony Pictures "reckon with" this problem?
Sony Pictures isn’t alone in having a predominantly white, predominantly male leadership, or paying its top executives multiples of what other employees make. But the numbers leaked in the recent hack – assuming they’re accurate – would mean that the top ranks of one major Hollywood studio are perhaps even less diverse than those of Silicon Valley tech companies and large Wall Street banks. After it patches up its security measures, that’s another problem Sony Pictures may have to reckon with.
Ust'-Ishim: Ancient DNA offers the first of what I expect in the coming years will be many disappointments to those emotionally invested in a SE Asian origin for K-M526
I don't expect the Hectors will gracefully accept their beating, but to others the presence of a previously unknown branch of K(xLT) in Siberia 45,000 years ago should be a pretty clear signal that the idea of a 500 year sprint from West or Central Asia to an already-inhabited SE Asia, followed, after an indefinite pause, by a repopulating of the world from Sundaland (if not the islands of Wallacea), all while failing to carry any trace of Denisovan admixture back to the future civilized world is an unnecessary and improbable fantasy.
The cline of Denisovan admixture, from faint, highly-selected remnants in mainland SE Asia to maxima among Melanesians and Australian Aborigines, has always pointed to gene flow into the region after its initial settlement rather than out of it, the K-bearers being one obvious candidate for the major source of this dilution. I'd also say it's more likely than not that they (an M526-carrying population of Central Asian origin) are the ones who brought culture to Hector's ancestors.
"EthnicMuse" is attempting to aggregate numbers that can't be aggregated, and the results lack face validity. T levels as measured by different techniques and/or at different laboratories are not in general directly intercomparable.
What do you think of this website and his analysis of testosterone levels in different racial groups?
Clinicians are being presented with normal male reference ranges for serum T from these automated platforms that have low end clinical limits down to 170–200 ng/dl (5.9–6.9 nmol/liter) and upper range limits of 700–800 ng/dl (24.3– 27.7 nmol/liter). These stated reference ranges provided by the manufacturer are significantly lower than the 300-1000 ng/dl (10.4–34.7 nmol/liter) reference range referred to in numerous publications over the past 30 yr based on tradi- tional RIA methods with or without the chromatography step as well as some research techniques employed by in- ternal recovery standards to correct for procedural losses (5).Differences that are to be expected between different assays and different laboratories, apart from any other factors, would likely swamp any anticipated racial differences in circulating testosterone levels. Between-study differences in collection times, sample handling, age and health condition of subjects, and so on, add further noise.
External quality control programs such as that provided by the College of American Pathologists allow laboratories to compare results with other laboratories using the same method or kit reagents. As shown in Table 1, the median value of a quality control sample (Y-04,2002) varied between 215 and 348 ng/dl (7.5 and 12.0 nmol/liter) among methods with coefficients of variation among laboratories using the same method or instrument ranging between 5.1% and 22.7%. The median average for this sample from all methods was 297 ng/dl (10.3 nmol/liter) and results were as low as 160 or as high as 508 ng/dl (5.5 to 17.6 nmol/liter). These results span the hypogonadal to eugonadal range.
[Measurement of Total Serum Testosterone in Adult Men: Comparison of Current Laboratory Methods Versus Liquid Chromatography-Tandem Mass Spectrometry]
I see that EM is at least vaguely aware of these issues, but he rationalizes publishing his "meta-analysis" as follows:
One cannot and should not compare different testosterone studies with different measurement methods. However, for the race-realist purpose of aggregating data, there is nothing inherently wrong with what the PDF file lists. If JP Rushton can use a few studies and make wild claims which are then used by the Internet-o-sphere, using 150 independent peer-reviewed sources with large samples is much more scientific than anything similar from the race realist community. [. . .]
Age differences will affect the results but healthy males should have negligible decreases. Assuming a 0.4% annual decline from 5000 pg/ml after age 40, a man at 80 should have 4275 pg/mL, less than a 15% difference if my spreadsheet math is correct. It would have been better to normalize for age. So while the tabled rankings is flawed, the point is that the entire issue is flawed as there is no standard measuring method in the first place. That race realists routinely use flawed data should be the issue but …
That blindly aggregating data from disparate studies (which in this realm I've never seen anyone other than EM attempt) is nonsensical does not mean all attempts at comparing circulating testosterone levels between races are "flawed". It means that if one wants to attempt such comparisons, one should focus on studies in which a single set of researchers, using standardized methods, publish results for multiple ethnic groups.
EM is aware, for example, of a study (pdf) in which blood samples from Swedes and Koreans "were analyzed in the same laboratory using the same assay". The result (in EM's words): "the Swedes had 25% more T than the Koreans in this study". I've seen other studies showing lower or similar levels of testosterone in East Asians compared to whites (and none showing anything like the 10% higher testosterone in East Asians asserted by EM). But EM apparently did not like where the data pointed (thus his version of "meta-analysis", in which valid data is swamped with garbage).
The rapid advance of sequencing technology, coupled with improvements in molecular methods for obtaining genetic data from ancient sources, holds the promise of producing a wealth of genomic data from time-separated individuals. However, the population-genetic properties of time-structured samples have not been extensively explored. Here, we consider the implications of temporal sampling for analyses of genetic differentiation and use a temporal coalescent framework to show that complex historical events such as size reductions, population replacements, and transient genetic barriers between populations leave a footprint of genetic differentiation that can be traced through history using temporal samples. Our results emphasize explicit consideration of the temporal structure when making inferences and indicate that genomic data from ancient individuals will greatly increase our ability to reconstruct population history.
In this paper we describe a method for estimating the age of rare genetic variants. These ages are highly informative about the extent and dates of connections between populations. Variants in closely related populations generally arose more recently than variants of the same frequency in more diverged populations. Therefore, comparing the ages of variants shared across different populations allows us to infer the dates of demographic events like population splits and bottlenecks. We also see that rare functional variants shared within populations tend to have more recent origins than nonfunctional variants, which is consistent with the effects of natural selection.
To better understand the spectrum of gene expression variation, alternative splicing, and the population genetics of regulatory variation in humans, we have sequenced the genomes, exomes, and transcriptomes of EBV transformed lymphoblastoid cell lines derived from 45 individuals in the Human Genome Diversity Panel (HGDP). The populations sampled span the geographic breadth of human migration history and include Namibian San, Mbuti Pygmies of the Democratic Republic of Congo, Algerian Mozabites, Pathan of Pakistan, Cambodians of East Asia, Yakut of Siberia, and Mayans of Mexico. We discover that approximately 25.0% of the variation in gene expression found amongst individuals can be attributed to population differences. However, we find few genes that are systematically differentially expressed among populations. Of this population-specific variation, 75.5% is due to expression rather than splicing variability, and we find few genes with strong evidence for differential splicing across populations. Allelic expression analyses indicate that previously mapped common regulatory variants identified in eight populations from the International Haplotype Map Phase 3 project have similar effects in our seven sampled HGDP populations, suggesting that the cellular effects of common variants are shared across diverse populations.
Parochial altruism, defined as increased ingroup favoritism and heightened outgroup hostility, is a widespread feature of human societies that affects altruistic cooperation and punishment behavior, particularly in intergroup conflicts. Humans tend to protect fellow group members and fight against outsiders, even at substantial costs for themselves. Testosterone modulates responses to competition and social threat, but its exact role in the context of parochial altruism remains controversial. Here, we investigated how testosterone influences altruistic punishment tendencies in the presence of an intergroup competition. Fifty male soccer fans played an ultimatum game (UG), in which they faced anonymous proposers that could either be a fan of the same soccer team (ingroup) or were fans of other teams (outgroups) that differed in the degree of social distance and enmity to the ingroup. The UG was played in two contexts with varying degrees of intergroup rivalry. Our data show that unfair offers were rejected more frequently than fair proposals and the frequency of altruistic punishment increased with increasing social distance to the outgroups. Adding an intergroup competition led to a further escalation of outgroup hostility and reduced punishment of unfair ingroup members. High testosterone levels were associated with a relatively increased ingroup favoritism and also a change towards enhanced outgroup hostility in the intergroup competition. High testosterone concentrations further predicted increased proposer generosity in interactions with the ingroup. Altogether, a significant relation between testosterone and parochial altruism could be demonstrated, but only in the presence of an intergroup competition. In human males, testosterone may promote group coherence in the face of external threat, even against the urge to selfishly maximize personal reward. In that way, our observation refutes the view that testosterone generally promotes antisocial behaviors and aggressive responses, but underlines its rather specific role in the fine-tuning of male social cognition.
Evolutionary explanations regarding the differential preference for particular traits hold that preferences arose due to traits’ association with increased potential for reproductive fitness. Assessments of physical attractiveness have been shown to be related to perceived and measured levels of health, an important fitness-related trait. Despite the robust association between physical attractiveness and health observed in the extant literature, a number of theoretical and methodological concerns remain. Specifically, the research in this area possesses a lack of specificity in terms of measures of health, a reliance on artificial social interactions in assessing physical attractiveness, a relatively infrequent use of non-student samples, and has left unaddressed the confounding effects of raters of attractiveness. Using these concerns as a springboard, the current study employed data from the National Longitudinal Study for Adolescent Health (N ≈ 15,000; aged 25 to 34 years) to assess the relationship between physical attractiveness and various specific and overall measures of health. Logistic and OLS regression models illustrated a robust association between physical attractiveness and various measures of health, controlling for a variety of confounding factors. In sum, the more attractive a respondent was rated, the less likely he or she was to report being diagnosed with a wide range of chronic diseases and neuropsychological disorders. Importantly, this finding was observed for both sexes. These analyses provide further support for physical attractiveness as a phenotypic marker of health. The findings are discussed in reference to evolutionary theory and the limitations of the study and future research suggestions are also addressed.
Dr James Higham, senior author, said: "Evolution produces adaptations that help animals thrive in a particular environment, and over time these adaptations lead to the evolution of new species.
"A key question is what mechanisms keep closely related species that overlap geographically from interbreeding, so that they are maintained as separate species.
"Our findings offer evidence for the use of visual signals to help ensure species recognition: species may evolve to look distinct specifically from the other species they are at risk of interbreeding with," Dr Higham said.
"In other words, how you end up looking is a function of how those around you look. With the primates we studied, this has a purpose: to strengthen reproductive isolation between populations."
1Stony Brook University, Stony Brook, New York, USA, 2University of Michigan, Ann Arbor, Michigan, USA
1Harvard Medical School, Boston, USA, 2Broad Institute, Cambridge, USA, 3Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany
As a first step, we have developed a statistical method for inferring segments of Neandertal local ancestry in modern humans and applied this method to construct a map of Neandertal ancestry in modern non-Africans, using data from Phase 1 of the 1000 genomes project combined with a high coverage (50×) Neandertal genome. This map reveals the adaptive impact of Neandertal gene flow as we find enhanced Neandertal ancestry in genes involved in keratin filament formation as well as other biological pathways. We also observe large regions with reduced Neandertal ancestry consistent with purifying selection against introgressing Neandertal alleles in part due to these alleles contributing to hybrid male sterility.
To extend this approach to other archaic-modern human introgression events, we generated deep genome sequences of 21 people from populations with substantial Denisovan ancestry: 16 Papua New Guineans, 2 Bougainville Islanders, and 3 aboriginal individuals from Australia. We also extend our method to infer Neandertal and Denisovan local ancestry in these populations. We test whether the same evidence for hybrid male sterility is observed in this introgression event as is observed between Neandertals and modern humans.
1Eco-anthropologie et Ethnobiologie, UMR 7206 CNRS, MNHN, Univ Paris Diderot, Sorbonne Paris Cité, F-75005, Paris, France, 2Max Planck Institute for Evolutionary Anthropology, Department of Evolutionary Genetics, Leipzig, Germany
SMBE 2014: Genome-wide ancestry patterns in Easter Islanders suggest a pre-European admixture event with Native Americans
1Centre for GeoGenetics. University of Copenhagen, Copenhagen, Denmark, 2Institute of Immunology. Oslo University Hospital. University of Oslo, Oslo, Norway, 3Center for Biological Sequence Analysis. Technical University of Denmark, Kongens Lyngby, Denmark
We have generated genome-wide data for 10 unrelated reputedly non-admixed Easter Islanders. By using non-parametric multidimensional statistics and clustering methods, we show genome-wide patterns consistent with both Native American and European admixture. We infer local Polynesian, Native American and European ancestry tracts and compare their length distributions to those expected under different demographic history models. We find more support for a model with Native American admixture event that predates a European admixture event. By masking the European and Native American ancestry tracts, we reconstruct the recent history of the Easter Island population compared to other existing genotyped Oceanic populations. These results provide additional detailed insight into the demographic history of Polynesian islanders revealing an outstanding event in recent human history.
SMBE 2014: Whole genome sequencing of an Ashkenazi Jewish reference panel supports population-targeted personal genomics and illuminates Jewish and European origins
1Columbia University, New York, NY, USA, 2Yale University, New Haven, CT, USA, 3The Feinstein Institute, Manhasset, NY, USA, 4The Zucker Hillside Hospital, Glen Oaks, NY, USA, 5Icahn School of Medicine at Mount Sinai, New York, NY, USA, 6Albert Einstein College of Medicine, New York, NY, USA, 7Memorial Sloan Kettering Cancer Center, New York, NY, USA, 8The Hebrew University of Jerusalem, Jerusalem, Israel, 9Beth Israel Medical Center, New York, NY, USA
Department of Genetics, Harvard Medical School, Boston, USA
National University of Ireland Galway, Galway, Connaught, Ireland
SMBE 2014: Genotyping of 390,000 SNPs in more than forty 3,000-9,000 year old humans from the ancient Russian steppe
1Harvard Medical School, Boston, MA, USA, 2Broad Institute of Harvard and MIT, Cambridge, MA, USA, 3Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany, 4Hartwick College, Oneonta, NY, USA
We applied the SNP capture as well as mitochondrial genome enrichment to a series of 65 bones dating to between 3,000-9,000 years ago from the Samara district of Russia in the far east of Europe, a region that has been suggested to be part of the Proto-Indo-European homeland. We successfully extracted nuclear data from 10-90% of targeted SNPs for more than 40 of the samples, and for all of these samples also obtained complete mitochondrial genomes. We report three key findings:
- Samples from the Samara region possess Ancient North Eurasian (ANE) admixture related to a recently published 24,000 year old Upper Paleolithic Siberian genome. This contrasts with both European agriculturalists and with European hunter-gatherers from Luxembourg and Iberia who had little such ancestry (Lazaridis et al. arXiv.org 2013). This suggests that European steppe groups may have been be implicated in the dispersal of ANE ancestry across Europe where it is currently pervasive.
- The mtDNA composition of the steppe population is primarily West Eurasian, in contrast with northwest Russian samples of this period (Der Sarkissian et al. PLoS Genetics 2013) where an East Eurasian presence is evident.
- Samara experienced major population turnovers over time: early samples (>6000 years) belong primarily to mtDNA haplogroups U4 and U5, typical of European hunter-gatherers but later ones include haplogroups W, H, T, I, K, J.
[Via Greg Cochran.]
ESHG 2014: Causal relationship of body mass index with cardiometabolic traits and events: a Mendelian randomization analysis
Keywords: body mass index; Mendelian randomization; Cardiometabolic
Authors: M. V. Holmes1,2, L. A. Lange3, T. Palmer4, M. B. Lanktree5, IBC BMI Mendelian Randomization Group, E. E. Schadt6, F. W. Asselbergs7,8,2, A. P. Reiner9,10, B. J. Keating1; 1University of Pennsylvania, Philadelphia, PA, United States, 2University College London, London, United Kingdom, 3University of North Carolina School of Medicine at Chapel Hill, Chapel Hill, NC, United States, 4University of Warwick, Warwick, United Kingdom, 5McMaster University, Hamilton, ON, Canada, 6Mount Sinai School of Medicine, New York, NY, United States, 7University Medical Center Utrecht, Utrecht, Netherlands, 8Durrer Center for Cardiogenetic Research, Utrecht, Netherlands, 9University of Virginia, Charlottesville, VA, United States, 10Fred Hutchinson Cancer Research Center, Seattle, WA, United States.
Abstract: Elevated body mass index (BMI) associates with cardiometabolic traits on observational analysis, yet the underlying causal relationships remain unclear. We conducted Mendelian randomization analyses using 14 SNPs associated with BMI from a recent discovery analysis to investigate the causal role of BMI with cardiometabolic traits. We used eight population-based cohorts, including 34,538 individuals of European ancestry with 4,407 type 2 diabetes (T2D), 6,073 coronary heart disease (CHD) and 3,813 stroke cases. A genetically-elevated one kg/m2 increase in BMI resulted in higher levels of fasting glucose, insulin, interleukin-6 and systolic blood pressure but reduced levels of HDL-C and LDL-C (values reported in Table). Apart from LDL-C, all causal estimates were directionally concordant to observational estimates. A genetically-elevated one kg/m2 increase in BMI increased odds of T2D but did not affect risk of CHD or stroke. A meta-analysis incorporating published studies with 27,465 CHD events in 219,423 individuals yielded a pooled odds ratio of 1.04 (95%CI: 0.97, 1.12) per 1 kg/m2 increase in BMI. In conclusion, we identified causal effects of BMI on several cardiometabolic traits, however whether BMI causally impacts on CHD risk requires further evidence.
ESHG 2014: Insights into the genetic architecture of anthropometric traits using whole genome sequence data
Keywords: body mass index; whole genome sequencing; association
Authors: E. Zeggini, UK10K consortium; Wellcome Trust Sanger Institute, Hinxton, United Kingdom.
Abstract: Body weight and fat distribution measures are associated with increased risk of cardiometabolic disease. As part of the UK10K study, we have investigated the genetic architecture of anthropometric traits in 3,538 individuals with 6.5x whole genome sequence (WGS) data from the ALSPAC and TwinsUK cohorts. Variants discovered through WGS, along with those from the 1000 Genomes Project (1KGP), were imputed into additional individuals from the ALSPAC and TwinsUK cohorts with GWAS data (total sample size 9,979). We investigated association between anthropometric traits and 8.6 million low frequency and common variants (MAF>0.01). We are in the process of obtaining in silico replication of prioritised signals. In interim replication analysis across ~15,000 samples, 43 out of 66 novel signals for BMI have the same direction of effect in the replication cohorts (p-value=0.0093). We examined the concordance of the direction of effect at established loci for each trait. Out of the 31 established independent loci for BMI that were present in our data, 28 have the same direction of effect (p-value=2.3e-06). For weight, 10 out of 11 known loci (p-value=0.006), and for height 151 out of 172 loci (p-value < 2.2e-16) have the same direction of effect, respectively. We estimated the improvement in genome-wide signal captured relative to those present in HapMap 2, HapMap 3 or 1KGP. We find no appreciable increase in variance explained as density increases, suggesting that the contribution of variants with MAF>0.01 are likely to be well-captured by existing GWAS implementation. Larger sample sizes will be required to refine these estimates.
ESHG 2014: The degree of Intellectual Disability is significantly associated with an excess of Runs of Homozygosity (ROH)
Keywords: Intellectual Disability; ROH
Authors: I. Gandin1,2, F. Faletra2, M. Carella3, V. Pecile2, G. Ferrero4, E. Belligni4, P. Palumbo3, O. Palumbo3, P. Bosco5, C. Romano5, C. Belcaro1, D. Vozzi2, A. P. d'Adamo1,2; 1University of Trieste, Trieste, Italy, 2IRCCS Burlo Garofolo, Trieste, Italy, 3IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo (FG), Italy, 4AO citta' della salute e della scienza, Torino, Italy, 5IRCCS Oasi Maria SS, Troina(EN), Italy.
Abstract: Several recent studies focused on the effect of extended homozygosity on highly complex and polygenic traits where recessive inheritance may play an important role. Since excess of homozygosity might increase the risk for disorders like schizophrenia, Alzheimer disease and autism, we have set out a study to investigate the effect of ROHs on the degree of Intellectual Disability (ID). About 370 unrelated individuals with ID were collected and classified into mild/moderate ID (MM-ID) for IQ ranging from 35-40 to 70-75 and severe/profound ID (SP-ID) for IQ below 35-40. High-density SNP array data were processed with the aim of detecting and analyze ROHs. Since different array platform were used, homozygosity and ROHs mean length were compared in MM-ID vs SP-ID separately in each dataset. Results were then combined for a meta-analysis. Our data revealed an association between the amount of homozygosity and the degree of ID, according to the recent findings on autism (Gamsiz et al., 2013). Accounting for principal components to control population stratification, we tested for ROHs mean length and detected significantly (p < 0.005) longer stretches in SP-ID compared to MM-ID. Weaker association was detected in burden ROH analysis, showing an increase of the percentage of genome covered by ROHs for SP-ID cases. Extent of ROHs seems to contribute to the pathogenesis of ID, suggesting that autosomal recessive variants have a crucial role on the modulation of the severity of ID that still need to be investigated.
ESHG 2014: Polygenic risk for ADHD is associated with impaired educational achievement and lower IQ in the general population
Keywords: ADHD; Polygenic scores; Educational attainment
Authors: E. Stergiakouli1, J. Martin2, M. L. Hamshere2, A. Thapar2, D. M. Evans1, N. J. Timpson1, G. Davey Smith1; 1MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, United Kingdom, 2MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Cardiff, United Kingdom.
High levels of ADHD symptoms during childhood carry risk of worse academic performance and can impact on employment and earnings in adulthood. Polygenic score analysis was used to show that common risk alleles for clinical ADHD contribute to the risk of having higher ADHD symptoms in the general population (Martin et al. in press). We have used polygenic score analysis to investigate the contribution of common risk variants for clinical ADHD on educational performance and IQ in the general population.
Academic performance was assessed using results from Key Stage 3 national tests and externally marked GCSE examinations in 6,385 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Polygenic risk scores were calculated for ALSPAC children and their mothers based on the results of an ADHD GWAS (Stergiakouli et al. 2012).
ADHD polygenic scores on the children were associated with worst educational outcomes as represented by both time points and also with lower IQ scores at age 15.5 (see Table). Moreover, ADHD polygenic scores on the mothers were associated with lower IQ in the mothers and worst educational outcomes in the children (see Table).
Our results suggest that the same genetic variants that are relevant for an ADHD diagnosis are also implicated in impaired academic performance in the general population and lower IQ score in both children and adults.