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r/iamverysmart
soonapu faction wen?
is over if ure not i am very smart in 2018
Between 69 and 420.
r/iamverysmart
IQ is a cope
Mogs me, I'm at 97 jflPeople who claim IQ doesn't matter are the real copers.
Mine is 98 by the way, so basically average.
82, had it tested in a psych ward.
Mogs me, I'm at 97 jfl
Slav actuallyEthnics I presume?
omg 1 whole point less. You will never beat me in life!
......not serious.
.....maybe a little bit serious.
Slav actually
John Kasich is ethnic? How about John Malkovich? Steve Novak? Steven Hauschka?Slavs are ethnics. No hate, just pointing it out.
How tf can everyone have an above average iq? That makes zero sense
tbh tbh...
Super Saiyan IQ
probably like 80, mexican andy is smarter and more capable than me
Childhood intelligence is heritable, highly polygenic and associated with FNBP1L
Intelligence in childhood, as measured by psychometric cognitive tests, is a strong predictor of many important life outcomes, including educational attainment, income, health and lifespan. Results from twin, family and adoption studies are consistent with general intelligence being highly heritable and genetically stable throughout the life course. No robustly associated genetic loci or variants for childhood intelligence have been reported. Here, we report the first genome-wide association study (GWAS) on childhood intelligence (age range 6-18 years) from 17,989 individuals in six discovery and three replication samples. Although no individual single-nucleotide polymorphisms (SNPs) were detected with genome-wide significance, we show that the aggregate effects of common SNPs explain 22-46% of phenotypic variation in childhood intelligence in the three largest cohorts (P=3.9 × 10(-15), 0.014 and 0.028). FNBP1L, previously reported to be the most significantly associated gene for adult intelligence, was also significantly associated with childhood intelligence (P=0.003). Polygenic prediction analyses resulted in a significant correlation between predictor and outcome in all replication cohorts. The proportion of childhood intelligence explained by the predictor reached 1.2% (P=6 × 10(-5)), 3.5% (P=10(-3)) and 0.5% (P=6 × 10(-5)) in three independent validation cohorts. Given the sample sizes, these genetic prediction results are consistent with expectations if the genetic architecture of childhood intelligence is like that of body mass index or height. Our study provides molecular support for the heritability and polygenic nature of childhood intelligence. Larger sample sizes will be required to detect individual variants with genome-wide significance.
In a sample of 25 pairs of EOS proband-healthy full sibling, we sought to investigate the association of KIBRA with memory performance. Episodic memory was measured using immediate and delayed recall measures of the California Verbal Learning Test. In a combined analysis (TT vs. TC/CC) assuming a C dominant model of inheritance, we found a main effect of genotype where individuals with TT genotype outperformed non-TT-carriers at immediate and delayed recall.
Moreover, among older adults T-allele carriers of the examined KIBRA polymorphism showed better spatial learning compared to C homozygotes. Together these findings provide the first evidence for an effect of the KIBRA rs17070145 polymorphism on spatial memory in humans and age differences in the reliance on landmark and boundary-related spatial information.
rs6087771
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Population Group Sample Size Ref Allele Alt Allele
Population Group Sample Size Ref Allele Alt Allele Total Global 17654 T=0.80650 C=0.19350, G=0.00000 European Sub 12466 T=0.82031 C=0.17969, G=0.00000 African Sub 1152 T=0.6094 C=0.3906, G=0.0000 African Others Sub 22 T=0.73 C=0.27, G=0.00 African American Sub 1130 T=0.6071 C=0.3929, G=0.0000 Asian Sub 158 T=1.000 C=0.000, G=0.000 East Asian Sub 102 T=1.000 C=0.000, G=0.000 Other Asian Sub 56 T=1.00 C=0.00, G=0.00 Latin American 1 Sub 208 T=0.760 C=0.240, G=0.000 Latin American 2 Sub 2520 T=0.8218 C=0.1782, G=0.0000 South Asian Sub 94 T=0.98 C=0.02, G=0.00 Other Sub 1056 T=0.7869 C=0.2131, G=0.0000
The strongest association for a maternal genetic effect was on chromosome 7 in the CHRM2 gene (rs6967953, hg18 chr7:g.136353916G>A, allele=A, S1=1.38, Wald P-value=6.01 × 10−6). This area has been previously linked with IQ and one of the strongest linkage signals reported for ASD occurred at 7q within 1.6 kb of the CHRM2 gene.36 One of our top hits for maternal genetic effects was identified on chromosome 22 in the SHANK3 gene (rs5770820, hg18 chr22:g.49497339G>A, allele =A, S1=1.25, Wald P-value=5.54 × 10−5, see Figure 1). Disruptions in the SHANK3 gene have been associated with autistic traits and in particular, these disruptions are responsible for the development of Phelan–McDermid syndrome and other non-syndromic ASDs.37 Figure 1 shows that there are no SNPs in high LD with rs5770820 (the SNP in highest LD was rs739365, R2=0.65) due to the limited number of SNPs common to all three arrays in the SSC data set.
Population | Group | Sample Size | Ref Allele | Alt Allele |
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Population | Group | Sample Size | Ref Allele | Alt Allele |
---|---|---|---|---|
Total | Global | 207126 | G=0.780438 | A=0.219562 |
European | Sub | 176176 | G=0.777319 | A=0.222681 |
African | Sub | 7770 | G=0.9284 | A=0.0716 |
African Others | Sub | 274 | G=0.934 | A=0.066 |
African American | Sub | 7496 | G=0.9282 | A=0.0718 |
Asian | Sub | 750 | G=0.535 | A=0.465 |
East Asian | Sub | 574 | G=0.542 | A=0.458 |
Other Asian | Sub | 176 | G=0.511 | A=0.489 |
Latin American 1 | Sub | 990 | G=0.822 | A=0.178 |
Latin American 2 | Sub | 9042 | G=0.7617 | A=0.2383 |
South Asian | Sub | 5056 | G=0.7290 | A=0.2710 |
Other | Sub | 7342 | G=0.7766 | A=0.2234 |
sub 80I've taken 2 tests. I took the Wechsler intelligence scale for children as a Freshman in High School and scored 149. I took an Wechsler Adult IQ test and scored 143.
sameBetween 69 and 420.