Special thanks to commenter Carl Churchill for bringing this to my attention. Finally genes for IQ are being officially found, and ten years sooner than I thought!
Previous research had found genes for IQ but those findings failed to replicate in followup studies. There also been studies finding genes for dementia, which I consider genes for IQ, given the high correlation between old age cognitive function and early life cognition. But this is the first study I know of that directly found genes for IQ and replicated the findings.
The authors of the study are G Davies, RE Marioni, DC Liewald, WD Hill, SP Hagenaars, SE Harris, SJ Ritchie M Luciano, C Fawns-Ritchie1, D Lyall , Cullen, SR Cox, C Hayward , DJ Porteous, J Evans , AM McIntosh, J Gallacher, N Craddock, JP Pell, DJ Smith, CR Gale,and IJ Deary.
Here’s the abstract:
People’s differences in cognitive functions are partly heritable and are associated with important life outcomes. Previous genomewide association (GWA) studies of cognitive functions have found evidence for polygenic effects yet, to date, there are few replicated genetic associations. Here we use data from the UK Biobank sample to investigate the genetic contributions to variation in tests of three cognitive functions and in educational attainment. GWA analyses were performed for verbal–numerical reasoning (N = 36 035), memory (N = 112 067), reaction time (N = 111 483) and for the attainment of a college or a university degree (N = 111 114). We report genome-wide significant single-nucleotide polymorphism (SNP)-based associations in 20 genomic regions, and significant gene-based findings in 46 regions. These include findings in the ATXN2, CYP2DG, APBA1 and CADM2 genes. We report replication of these hits in published GWA studies of cognitive function, educational attainment and childhood intelligence. There is also replication, in UK Biobank, of SNP hits reported previously in GWA studies of educational attainment and cognitive function. GCTA-GREML analyses, using common SNPs (minor allele frequency40.01), indicated significant SNP-based heritabilities of 31% (s.e.m. = 1.8%) for verbal–numerical reasoning, 5% (s.e.m. = 0.6%) for memory, 11% (s.e.m. = 0.6%) for reaction time and 21% (s.e.m. = 0.6%) for educational attainment. Polygenic score analyses indicate that up to 5% of the variance in cognitive test scores can be predicted in an independent cohort. The genomic regions identified include several novel loci, some of which have been associated with intracranial volume, neurodegeneration, Alzheimer’s disease and schizophrenia.
Of course critics like commenter Chartreuse can still argue that these are only local genetic effects, so they need to be replicated in very different countries to prove they have an independent effect on IQ, but typically, with other traits, genes that are replicated in one population are replicated in very different continents and cultures, given enough sample size. I suspect the same will happen with IQ.
where’s the replication fucktard?
but typically, with other traits, genes that are replicated in one population are replicated in very different continents and cultures, given enough sample size.
yet more lies.
published GWA studies of cognitive function.
and they are?
and given that there are only 20,000 genes one would expect “replication” if 10,000 of those have an effect.
and that “replication” would be totally meaningless.
how fucking retarded is peepee?
i know she’s a transgendered chinaman, who is gay for steve shoe, but this post takes the cake for not understanding what “replication” means.
Why do you almost never have on topic shit to say? Could you not find a more clever insult than “Peepee” Are you two??????
replication means replication for the set of genes when there are a lot of them.
“replication” of individual genes in a large set is going to happen just by chance if that set is sufficiently large.
duh.
Not only are you a premorbid schizophrenic, but apparently you can’t read:
Polygenic score analyses indicate that up to 5% of the variance in cognitive test scores can be predicted in an independent cohort.
not only are you a premorbid schizophrenic but apparently you think i can’t read.
this quote is totally MEANINGLESS.
YOUR ABOVE RESPONSE IS 100% IRRELEVANT TO MY COMMENT.
YOU SHOULD LEARN WHAT “REPRODUCIBLE” MEANS PEEPEE THE CHINK.
https://en.wikipedia.org/wiki/Reproducibility
https://en.wikipedia.org/wiki/Replication_crisis
this might be another example of peepee’s mathematical retardation.
she apparently doesn’t understand that it is this very predictive-ness which is used to identify the alleles in the first place.
as Misdreavus said:
“Dunning-Kruger as fuck…
i only read this blog for jorge videla…”
I understood more about math in the 7th grade than either you or Misdreavus understand today.
You are shifting the goal posts, as all dishonest debaters do
Replication means replication means replication
no shifting peepeetard.
let’s do a reductio ad absurdum…
imagine that for 100 years a total of 1,000,000 scientists have looked for alleles for IQ.
it is now the year 2116.
do you think some of them would have found the same alleles?
do you think such a concordance would have any significance at all?
humans only have 20,000 genes peepee.
don’t make me attach electrodes to your labia.
Then you should have set a higher standard than mere replication. By the very standard you defined, HBD has been vindicated. So what now is the standard?
now YOU are lying about what i’ve said.
peepeetard…there IS an allele which is strongly associated with MIs.
that population with the highest frequency for this allele lives in New Guinea.
these folks don’t have MIs, even when they live long enough.
get it?
ONE DIS-CONFIRMATION DISPROVES AN INDEPENDENT GENETIC EFFECT.
THE SAME IS TRUE FOR THE PIMA AND THE TONGANS. THREE GENERATIONS BACK NONE HAD DIABETES. NOW THEY HAVE THE HIGHEST RATE IN THE WORLD…EXCEPT THE PIMA THAT LIVE ACROSS THE BORDER IN MEXICO. THEIR RATE IS LOWER THAN THAT OF WHITE AMERICANS.
THE SAME IS TRUE FOR SZC.
MELANESIANS LIVING WESTERNIZED LIVES HAVE THE SAME RATE AS WETSTERNERS. THOSE LIVING AS THEY HAD LIVED UNTIL COLONIZATION…ALMOST NONE HAVE SCZ.
I’M GOING TO THROW YOU OUT OF AN AIRPLANE.
chartreuse
The reproducibility crisis is for everything BUT IQ in psychology. See Steven Pinker.
i thought i remembered a post on shoe’s blog about “the first hits for cognitive ability” less than 1 y ago.
anyway, after i’ve thrown santa claus out of an airplane, i’ll read the study in full.
for what population was the “replication” explaining 5%?
how big was the expected %? sounds like it was 32%, not 5%. whoops.
how different were the independent and dependent populations?
They are largely British samples because to find SNPs you need large samples from homogenous groups
i think they only have to be homogeneous when they’re within the same country.
and the reason is to avoid caste systems and the effects of discrimination, etc.
and yes the sample is 100% white british, and this is the sngle largest study of its kind to date.
yet prof shoe has yet to hear of it apparently.
i believe this is the money shot, but i’m not sure what it means:
We present lookups for all
available SNPs, as not all SNPs from the current study were
available due to differences in imputation reference panels. We
find that, of the 1115 genome-wide significant SNPs associated
with educational attainment, 327 (general cognitive function), 326
(years of education), 326 (college degree) and 267 (childhood
intelligence) were available in the published GWAS. Of these 158,
240, 211 and 47, respectively, showed replication at P < 0.05, for
general cognitive function, years of education, college degree and
childhood cognitive function.
i thought they just compared sets of genes or SNPs or whatever that belonged to the set {x: differences in x are associated with differences in phenotype & the association is so strong it is very unlikely to be due to chance} for the current study and past studies as long as their “reference panels” were the same, so i don’t know what P < 0.05 means. i don't think this refers to the P values of the published hits.
and how much of the genome was looked at?
according to shoe the sample size is close to being enough to identify a lot more than 5% of the variance.
Biobank samples were genotyped using either the
UK Bileve (N = 49 979) or the UK Biobank axiom array (N = 102 750).
how close does this come to sample of the whole genome for anything that might have an effect, ignoring the “junk DNA”, etc.?
and “replication” of one allele doesn’t mean replication some of the time and not others.
if there is an independent genetic effect, “replication” means the allele is always replicated,
always…
provided it has a sufficient frequency in the population.
when these bozos give p values of 1 in 1,000,000 or whetever, then every study of the same size should find this allele. every single one. and they don’t need to be bigger. they don’t need to have a sample size of 1,000,000.
Read the section about replication, chartreuse.
Replication is reported where Po0.05
in the UK Biobank GWASs. For the 13 genome-wide significant
SNPs in the 2015 GWAS of general cognitive function,13 11 SNPs in
the chromosome 6 region were replicated for educational
attainment, and verbal–numerical reasoning. A single SNP on
chromosome 14 (rs17522122 in the AKAP6 gene) was replicated in
verbal–numerical reasoning, RT, and memory. Of the three
memory hits reported by Debette et al.,20 one SNP (rs4420638
in the APOC1 gene) replicated in the UK Biobank memory GWAS.
Of the three educational attainment SNP hits (two for college
degree, rs11584700, rs4851266; one for years of education,
rs9320913) reported by Rietveld et al.,
24 all three replicated in
UK Biobank for educational attainment, and two SNPs, rs4851266
and rs9320913, also replicated for verbal–numerical reasoning. Of
the three SNPs associated with educational attainment and
cognitive function (rs1487441, rs7923609 and rs2721173) in
Rietveld et al.,
23 all demonstrated replication with educational
attainment in UK Biobank, rs1487441 and rs2721173 with verbal–
numerical reasoning, and rs2721173 with RT.
Of the 21 genome-wide significant hits reported in the most
recent Alzheimer’s disease GWAS, one SNP, rs983392, showed
replication with memory in UK Biobank.
One SNP, rs17689882, in the CRHR1 gene that was associated
with intracranial volume37 was replicated in UK Biobank
with both educational attainment and verbal–numerical
reasoning.
For the gene-based lookups, the HMGN1 gene reported in the
general cognitive function paper13 did not replicate for any of the
traits (Supplementary Table S7). The FNBP1L gene, which has been
associated with childhood cognitive ability,35 was replicated in the
educational attainment analysis (P = 0.004). Of the seven genebased
hits for educational attainment24 (college versus no
college), two (PIK3C2B and TET2) were replicated in UK Biobank
for the educational attainment variable. None of the genes was
replicated for the other three traits. For the years of education
variable examined by Rietveld et al.,
24 12 out of the 16 significant
genes were replicated in the UK Biobank educational attainment
analysis. Five of these genes also replicated for verbal–numerical
reasoning. There was no overlap for the RT or memory traits. Of
the genes linked to educational attainment and cognitive function
in Rietveld et al.,23 NRXN1 was associated with verbal–numerical
reasoning and POU3F2 with memory in UK Biobank.
i’m thinking Rietveld is a sample from a very similar population.
but what fraction of Deary et al’s hits are “replicated” really?
in order to answer this requires comparing the number of hits with the number of hits…
that is, the number from the current study with that from other studies…of a significantly different population.
if the number of hits is large for the current study…one should expect that these will overlap with some hits from other studies just by chance.
11 SNPs in the chromosome 6 region were replicated for educational
attainment, and verbal–numerical reasoning.
again, why just one chromosome?
i have already expressed my conviction that the set of genes or the set of sets of genes which influence IQ, in the HARD sense, irrespective of time and place, will not be null…but it will be SMALL…and its total effect will account for less than 50% of the variance.
I haven’t read the paper yet myself, but I suspect some of these genes have been replicated almost more than once, because not only have they been linked to IQ in two different samples, but it sounds like they’ve been linked to proxies for IQ in other samples (i.e. dementia, brain size)
what peepeetard didn’t tell all y’all from the paper:
None of the 36 SNPs associated with RT replicated in any of the above-listed
published GWAS.
so much for her “chrometric” scores.
The largest proportion of variance explained in
LBC1936 was 5.4% for a vocabulary-based test (the National Adult
Reading Test) 61 using the Educational Attainment polygenic score
with a SNP inclusion threshold of all SNPs from the GWAS.
so much for her “chrometric” scores.
It’s chronometric. Chronometric scores might not be that heritable when you first play. There have been brilliant people who were below average at chronometrics in their first 50 tries, but their MAXIMUM scores have been far more impressive than the maximum scores of 99.9% of Americans their age. Once you progress to your physiological limit, you seem to hit a hard wired genetic wall.
Also, reaction time speed is much less g loaded than reaction time consistency. I don’t know if this study even measured the latter but the software I played on gave it great weight.
Can you name/link the software, please?
They no longer sell it.
For verbal–numerical reasoning we
report 149 SNPs reaching genome-wide significance; 37 were
available for general cognitive function, years of education and
college degree, and 29 for childhood intelligence. Thirty-six SNPs
in the chromosome 22 region replicate for general cognitive
function, one SNP on chromosome 7 demonstrated replication
with childhood intelligence, and no replication was observed
with either years of education or college degree.
so iiuc, 36 out of 37 “available” hits were matched by this study. if that’s right, then i would consider this one instance of replication. but i’m not sure iiuc, and why are they all on one chromosome?
maybe carltard could explain.
The most significant finding for verbal–numerical reasoning was for a gene-dense
region on chromosome 22, and replication of this region was
observed with general cognitive function. This region contains the
cytochrome P450 gene (CYP2D6), which uses hydroxytryptamines
(such as serotonin) and neurosteroids as endogenous substrates64
and may explain some of the links between cognitive functions
and mental illnesses. Given the associations of this region with
drug metabolism, it would be interesting to investigate this
finding further with specific reference to medication use and
psychiatric disease history. Brain size and cognitive ability are
correlated phenotypically,65 and the significant hit in the GWAS of
intracranial volume37 was also significant in SNP- and gene-based
analyses in the present study.
The
strongest signal was on chromosome 22 in a region that includes:
the cytochrome P450 gene CYP2D6, which is linked to
drug metabolism; NADH dehydrogenase (ubiquinone) 1 alpha
subcomplex, 6, 14 kDa (NDUFA6), which is involved in mitochondrial
function;46 and septin 3 (SEPT3), which is associated
with Alzheimer’s disease.47 The two other regions included: SNPs
in phosphodiesterase 1C, calmodulin-dependent 70 kDa (PDE1C),
a calmodulin-dependent PDE that is stimulated by a calciumcalmodulin
complex;48 and a single SNP in Fucosyltransferase 8
(alpha (1,6) fucosyltransferase (FUT8), which catalyses the transfer
of fucose from GDP-fucose to N-linked type complex glycopeptides.49
These were on chromosomes 7 and 14, respectively.
The gene-based analysis of verbal–numerical reasoning identi-
fied 17 significant genes from across seven regions, including
multiple hits on chromosome 22, such as SEPT3, CYP2D6 and
NDUFA6 (Supplementary Table S3). Other gene-based hits linked
to neurobiological pathways include: Ataxin2-like (ATXN2L) on
chromosome 16 (a member of the spinocerebellar ataxia family
which is associated with neurodegenerative disorders); amyloid
beta (A4) Precursor Protein-Binding, Family A, Member 1(APBA1)
on chromosome 9, which interacts with the Alzheimer’s disease
amyloid precursor protein;50 and SH2B Adaptor Protein 1 (SH2B1)
on chromosome 16, previously associated with type 2 diabetes.51
The proportion of variance in verbal–numerical reasoning that
was explained by all common genetic variants was 31% (GCTAGREML
estimate 0.31, s.e.m. = 0.018) (Table 1).
CONCLUSIONS—The much lower prevalence of type 2 diabetes and obesity in the Pima Indians in Mexico than in the U.S. indicates that even in populations genetically prone to these conditions, their development is determined mostly by environmental circumstances, thereby suggesting that type 2 diabetes is largely preventable. This study provides compelling evidence that changes in lifestyle associated with Westernization play a major role in the global epidemic of type 2 diabetes.
http://care.diabetesjournals.org/content/29/8/1866.full
http://wrongplanet.net/forums/viewtopic.php?t=157531
This comments are disgusting, someone need to say to this retarded that they are not superior than other people, what they love to say ”just different”.
Idiotic people with enormous, WRONG and repulsive ego, so-called ”liberals/socialist/communist//”, a lot of them.
Environmental fluctuation don’t mean that don’t exist genes role, are not ALL of amerindians who are becoming diabetic. This mean something…
If you think that it’s a ”prove” that environment are magnanimously superior than genes i think you must need re-think your hasty beliefs.
no. brazilian fucktard. E is not superior to G, nor is G superior to E.
the human being with rare exceptions is a cake: flour, eggs, butter, etc.
but is not flour + eggs + butter.
get it?
http://www.ncbi.nlm.nih.gov/pubmed/6609726
Only two overtly insane chronic schizophrenics were found among over 65,000 examined or closely observed adults in remote regions of Papua New Guinea (PNG, 1950-1967) and Malaita , Solomon Islands (1980-1981), and on Yap , Micronesia (1947-1948). In preneuroleptic Europe over 130 would have been expected. When these peoples became partially westernized and consumed wheat, barley beer, and rice, the prevalence reached European levels.
you need to find a bathhouse and stick with it.
i will put electrodes on your dick, and throw you into the Parana alive from 10,000 ft.
”no. brazilian fucktard. E is not superior to G, nor is G superior to E.”
Shut up, learn to talk correctly with people, dementia!!
”you need to find a bathhouse and stick with it.
i will put electrodes on your dick, and throw you into the Parana alive from 10,000 ft.”
so, your mental defect in emotion and empathy is (excuse for drunktards) EQUALLLLLLLLLLLLLL environmental and genes…
the eternal ”equaaaaaaality” in defective brains….
words no have sense in your putrid mouth, i really hate emotionally idiotic people like you,
I THINK YOU’RE VERY DEPRESSED…
think in suicide, will be good for you,
AND FOR USSSSSSS
true eugenics will wipe out on earth surface subhumans like you.
iqtard idiotic.
”Environmental fluctuation don’t mean that don’t exist genes role, are not ALL of amerindians who are becoming diabetic. This mean something…”
answer like a NORMAL people and without alcohol in your defective head, loser.
Environmental fluctuations affect people differently ‘CAUSE people are different.
”western levels of schizophrenia = 1%”
1% of people in this area become schizo after westernization.
1% AND not 30 or any other real greater change.
some people BORN schizophrenic as well some people BORN with diabetes type 1, a inborn ones. Other people are LIKELY to become schizo or diabetic cause wrong path-life with circumstances. And some people seems to be VERY LIKELY to become like that. nothing more.
some people BORN a drunktard retarded like you.
is that YOUR picture santa claus?
now i feel like a chimo.
and of course you would be partially right santa claus…
if the Pima and the Melanesians had higher rates of diabetes or the same rates of SCZ when compared to other ethnic groups living in the same fashion.
but ONLY partially.
why?
because in order to claim that P = G + E applies even in these environments, one would have to claim that diabetes and SCZ are quantitative traits/continuous traits.
insulin sensitivity does have a much wider span than merely diabetic or not diabetic, so the phenotype of insulin sensitivity might be substituted for the binary, diabetic/not diabetic.
SCZ on the other hand…this really is a binary phenotype. you hear voices or you don’t.
so…
1. P = G + E in the case of SCZ is FALSE.
2. P = G + E in the case of insulin sensitivity or fasting blood glucose level might still be true…but there aren’t any studies.
3. P = G + E is FALSE in the case of adiposity and blood pressure as these are traits with a lower bound, and all may attain this lower bound.
Is a picture of your HISPANIC daughter.
”and of course you would be partially right santa claus…
if the Pima and the Melanesians had higher rates of diabetes or the same rates of SCZ when compared to other ethnic groups living in the same fashion.”
anham
”insulin sensitivity does have a much wider span than merely diabetic or not diabetic, so the phenotype of insulin sensitivity might be substituted for the binary, diabetic/not diabetic.”
What the part i told that this is a binary case***
where****
but even if is not a ”bi-”nary case
many-to-most diabetic type 2 people tend to born in families with people who share heterozygotic versions.
same way schizophrenic tend to born in families with more cases of partial or 1/3 of schizo-traits.
where there smoke there fire.
A minority people born with higher environmental sensibility and most people born tend to born biologically robust.
Evolution and adaptation work like that, with a minority of potential new paths and majority with people ”who born” to sustain the population robustely.
You are entitled to your view, but just as a brief response to this sort of comment, genetic variation does affect our traits, all our traits, though always in a context-dependent way (and that includes genomic and external ‘environment’). As typical, when many genome regions contribute their effects are approximately additive in a statistical sense. How genetic mechanisms can actually be truly additive is a separate biochemical question. The apparent additivity of results is partly due to the way that analysis is done, such as the statistical modeling used, mainly for convenience because interactions are exceedingly difficult to parameterize convincingly much less to demonstrate statistically with available samples and under realistic assumptions. It is in a sense for the satisfaction of vested interests that some authors stress additivity, because prediction would not be very efficacious otherwise, because this relates to the degree to which retrospective sample-dependent additivity justifies extrapolation of the same results into the future; the record is pretty full and clear about that.
Thank you for the educated comment.
in order to understand that P != G + E may require The Navy Mechanics School.
if i think i float and you think i float, it happens.
https://en.wikipedia.org/wiki/Navy_Petty-Officers_School_of_Mechanics
condign punishment for HBDers.
You quote 1984********
chutzpah!!!!
robustely or stoutly
Schizophrenia
Diabetes
Homosexuality
Leftism
Based on many studies about neurological differences between leftists, moderates and conservatives a one difference is particularly interesting, amigdala.
I read now a study where the researchers found that rats with little brain amigdalas show very reduced capacity to detect predators.
Leftists tend to have little amigdalas too than conservatives, a primitive but essential part of the brain.
We live in a world where we need prove scientifically truims which are very very obvious, like leftism “madness”. Most part of artists are not designed to govern a nation.
One of these very obvious truism is exactly the incapacity of typical leftist to detect dangers. Why?? If you need a scientific explanation. Because they have little amigdalas, the fundamental part of brain that is responsible to survive.
In a decent world most of leftists must be diagnosed as borderline clinically unable as happen with ADHD or other to do certain activities like:
– engage in politics
ADHD have lack of attention and hyperactive
Autism have sensorial oversensitivity
Etc etc etc
And leftism have lack of survive skills, capacity to detect danger. A very problematic issue. So problematic than autism sensorial oversensitivity or ADHD attention deficit.
i really doubt that study was replicated.
iirc one study found some diagnosed as autistic had larger amygdala and another that there was no difference.
don’t take ANY results from the social sciences without a grain of salt like this:
econ, psychology, sociology, anthropology, political science…these are all 99% pseudo-science.
now santa claus…
when do you want task unit 2 to disappear you?
i can arrange for an 8 am Sao Paulo time pick up.
tell me and i’ll make sure my battery has plenty of juice for the session.
If psychology, sociology etc et all are pseudo-science
….
WHY you’re using constantly this studies to ”prove” ”your” points****
R
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T
A
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D
E
D
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P
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You must kill yourself
”emotions” dominate you all the time,
typical from goyish dumb.
Sorry, your small cortex did not allow you realize that one of amidgala functions is to recognize NATURAL predators, in human relations, you need the cortex to distinguish what is right from wrong.
Also, its proved that conservatives have on average 10 IQ less than liberals.
You are talking with me*
Promote islamofilia to embrace mass immigration of muslims and the same time promote woman and homossexual ”rights” for you = give the right judgment about this situation***
First, why promote mass immigration in Europe*
the most important, why a little Baghdad in Helsinki**
i still searching for REAL smart leftoids, is difficult!!!
What is incredibly irritating about this beasts is that they are extremely arrogant even when they are very wrong about everything if not in the begining of the argument no doubt that they will be wrong during the development of their pressuposts.
And with interpretation deficits.
I only come to this blog for the comment section
So, you’re using pseudo-scientific studies to prove your pseudo-scientific points**
You do not have the capacity to produce a sequential thinking, you’re really an idiot.
Do not blame the alcohol, is a birth defect, you was born as a loser.
As my emotionally retarded brother.
Your supposed ” super high iq ” does not mean anything if you do not know how to use it and for what
or you are a pathological liar (retarded) or you are just a moron with the only alleged evidence of genius (retarded). As smart as one Vos Savant ***
The few truisms that you say in relation to philosophy, quote other thinkers. I agree but you claim moral superiority AND************
what you’re doing here*****
to be morally superior is to be unpleasant with people who you never saw in your life****
The rest is a disaster.
As a good part of the most intelligent Leftists, an excess of white matter in the prefrontal cortex **
like a emotionally umbalanced woman, you’re a histerical. guti guti
”i really doubt that study was replicated.
iirc one study found *some* diagnosed as autistic had larger amygdala and another that there was no difference.”
tend to have….
This study is being replicated, sorry.
A lot of autistics are conservatives and i no doubt if many of this type are pro-white nationalism or advocacy.
when we are talking about populations we are talking about average’s, i hope you already know. Seems, the neuro-demographic epicenter of autistics, specially the asperger variety, is likely that will produce a left-leaning people if aspies and humanities students, specially the brightest among them, tend to have many similarities like higher verbal iq and lower non-verbal, specially spatial iq, higher empathy (while autistics are lower in sympathy)
Interestingly amygdala is also correlative or responsible for social complex behavior, i know many this social behavior which are idiotic like learn to pay greater attention to bullshit like religion but the rest…
Higher empathy OF COURSE when you agree 99,99% with them.
nothing new in the human-kind fauna !!!
http://www.dana.org/News/Details.aspx?id=42898
Although the amygdala appears to be involved in processing positive emotions, it is better known for its role in processing fearful and anxious emotional states associated with potential threats to survival. Animals whose amygdalas are experimentally damaged often lose their usual caution in the presence of strangers, even predators. In the classic demonstration, a rat whose amygdala has been removed will calmly approach even a sleeping cat. Humans with damaged amygdalas also show a blunted ability to react to things in the environment that would normally produce an emotional reaction.
Most HBDers do not really admire the cognitive abilities of Jews or their wealth as an output. They disdain them for their excesses, the same way they disdain blacks and East Asians for their behavioral flaws, which is also excessive in quality (too dumb, too smart, too passive or too aggressive). In essence, HBD demonstrates White supremacy and its equilibrium quality.