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Serious This is what your oneitis is up to right now

  • Thread starter 5ft4ropeconnoisseur
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5ft4ropeconnoisseur

5ft4ropeconnoisseur

My Stacy GF
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Apr 4, 2022
Posts
7,065
1697430479560


Thoughts? :feelsjuice:
 
No thoughts to be honest my head is empty
 
more likely it's several foids getting cummed on by 1 chadrone
 
I have no oneitus, but that is retarded jfl
 
Oneitis is unhealthy. It's unfamiliar to me though.

1697642646632

1697642672446

1697642706649
 
how is THAT even possible? Must be fake
 
She was already aware of it.

1697642706649
 
No no no ... This can't be true.
 

Oh. Hailee.

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.

Yes...

1697657658617


*In addition to the standard quality controls, for the TEDS cohort we removed SNPs if the info statistic (IMPUTE2 imputation package) in TEDS and WTCC2 controls < 0.98 (for SNPs that were imputed from HapMap) and < 0.90 (for SNPs that were imputed from HapMap and WTCC2 controls). We removed 927,192 SNPs following this exclusion.

Supplementary Table 2. The effect size of the top 100 SNPs (discovery + replication cohorts) sorted based on the association P-value. The direction was ordered as QIMR, ALSPAC, LBC21, LBC36, RAINE, TEDS, NTR, GenR, and UMN. 0 indicates that the effect size is zero.​


SUPPLEMENTARY NOTE​

The calculation of the average effective sample size from each cohort​

As part of the quality controls (QC) procedure, we calculated the average effective sample size (N) per cohort as a function of the allele frequency (p) and the standard error of the effect size (se) from the association test as , where m is the number of SNPs and Rsq is the imputation quality score.



This formula was derived from linear regression theory, where the sampling variance of an estimate of a regression coefficient from a model y = m + b*x + e is var(b) = se2(b) = 2 / (x2). If y is standardised to unit variance (as in our study), b is small and x a random variable then the sampling variance is approximately 1 / [N*var(x)]. From quantitative genetics theory, the variance of x is 2*p*(1-p), assuming Hardy-Weinberg equilibrium. With imputed data, this variance is reduced by a fraction of Rsq, where Rsq is the imputation accuracy. Hence, in total we get se2(b) ~ 1/ [N * Rsq * 2 * p * (1-p)]. The effective sample size (N) calculated accordingly.

Study Cohort Information​

Avon Longitudinal Study of Parents and Children (ALSPAC)​

Cohort description: ALSPAC is a population based longitudinal pregnancy-ascertained birth-cohort in the Bristol area of the UK. Specifically, recruitment sought to enrol all pregnant women with an estimated delivery date between 1st April 1991 and 31st December 19921, who where residents within three Health Districts of the former administrative county of Avon2. The initial cohort included 14,541 pregnancies and additional children eligible using the original enrolment definition were recruited up to the age of 18 years, increasing the total number of pregnancies to 15,247 (4.1% Non-White mothers). Information on the children from these pregnancies is available from questionnaires, clinical assessments, linkage to health and administrative records as well as biological samples including genetic and epigenetic information. Ethical approval was obtained from the ALSPAC Law and Ethics Committee (IRB00003312) and the Local Research Ethics Committees, and written informed consent was provided by all parents.

Intelligence measure: Intelligence in ALSPAC children at the age of 8 years was measured with the Wechsler Intelligence Scale for Children (WISC-III). A short version of the test consisting of alternate items only (except the Coding task) was applied by trained psychologists. Verbal (information, similarities, arithmetic, vocabulary, comprehension) and performance (picture completion, coding, picture arrangement, block design, object assembly) subscales were administered, each subtest was age-scaled according to population norms and a summary score for total IQ derived. Pertinent to this analysis, we generated sex and principal component (i.e. the two most significant principal components from Eigenstrat analysis, see below) adjusted Z-standardised intelligence quotient (IQ) scores for independent ALSPAC children with information on total IQ and genome-wide data. For this, IQ scores within a range of ±4SD relative to the total ALSPAC sample were regressed on sex (coded as 1 = male and 2 = female) and the principal components. The residuals were Z-transformed and subjected to genome-wide analysis.

Quality Controls (QCs): ALSPAC children were genotyped using the Illumina HumanHap550 quad chip genotyping platforms by 23andme subcontracting the Wellcome Trust Sanger Institute, Cambridge, UK and the Laboratory Corporation of America, Burlington, NC, US. The resulting raw genome-wide data were subjected to standard quality control methods. Individuals were excluded on the basis of gender mismatches; minimal or excessive heterozygosity; disproportionate levels of individual missingness (>3%), cryptic relatedness measured as proportion of identity by descent (IBD > 0.1) and insufficient sample replication (IBD < 0.8). The remaining individuals were assessed for evidence of population stratification by multidimensional scaling analysis and compared with Hapmap II (release 22) European descent (CEU), Han Chinese, Japanese and Yoruba reference populations; all individuals with non-European ancestry were removed. Hidden population stratification was thereafter controlled for by using EIGENSTRAT3 derived ancestry informative principal components scores. SNPs with a minor allele frequency of < 1%, a call rate of < 95% or evidence for violations of Hardy-Weinberg equilibrium (P < 5E-7) were removed.

Statistical analysis/additional information: Genotypic data were subsequently imputed using Markov Chain Haplotyping software (MACH v.1.0.16)4 and phased haplotype data from CEU individuals (Hapmap release 22, Phase II NCBI B36, dbSNP 126) based on a cleaned dataset of 9545 individuals and 464,311 autosomal SNPs. For the current analysis, the sample was restricted to a subset of 8365 independent individuals with imputed genotypes, 5517 of which also had phenotype data. Assuming an additive genetic disease model, association analysis was performed on imputed SNP data markers using Mach2QTL (v.108) software.

Acknowledgments: The UK Medical Research Council and the Wellcome Trust (WT092731/Z/10/Z), and the University of Bristol provided core support for the Avon Longitudinal Study of Parents and Children (ALSPAC). DME is supported by a Medical Research Council New Investigator Award (MRC G0800582 to D.M.E). JPK is funded by a Wellcome Trust 4-year PhD studentship (WT083431MA). We are extremely grateful to all the families who took part in the ALSPAC study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionist and nurses. We thank the Sample Logistics and Genotyping Facilities at the Wellcome Trust Sanger Institute and also 23andMe for generating the ALSPAC genome-wide data. This publication is the work of the authors and they will serve as guarantors for the contents of this paper.

Lothian Birth Cohort 1921 (LBC1921)​

Cohort description: The LBC1921 is a longitudinal study of healthy ageing, with a focus on cognitive ageing. The sample comprises 550 relatively healthy, community-dwelling individuals and was recruited between 1999 and 2001. Recruitment and testing are fully described elsewhere5, and a recent cohort profile article6 describes the data that have been collected to date. They were all born in 1921. Most took part in the Scottish Mental Survey 1932 (SMS1932) which took place on 1st June 1932 and applied the Moray House Test No. 12 (MHT) to almost everyone born in 1921 (95% of the population; N = 87,498). The SMS1932 was conducted by the Scottish Council for Research in Education, who permitted access to the childhood intelligence data. For the present study, only the childhood MHT scores are used. These were available for 464 subjects, whose mean (SD) age was 10.9 years (0.28) when they sat the test.

Intelligence measure: The measure of general intelligence was the Moray House Test No. 12. This is one of a series of tests of general intelligence devised by Godfrey Thomson at the Moray House College, University of Edinburgh, from the late 1920s onwards. The MHT is a group test of intelligence. It has 71 items and a maximum possible score of 76. It has a time limit of 45 minutes. It was also known as the ‘Verbal Test’ because the items have a predominance of verbal reasoning. The test has a variety of items, as follows: following directions (14 items), same–opposites (11), word classification (10), analogies (8), practical items (6), reasoning (5), proverbs (4), arithmetic (4), spatial items (4), mixed sentences (3), cypher decoding (2), and other items (4). Following the SMS1932, 500 boys and 500 girls were tested on the Stanford Revision of the Binet Test, to provide concurrent validity. The MHT-Binet correlations were 0.81 for the boys and 0.78 for the girls7.

Lothian Birth Cohort 1936 (LBC1936)​

Cohort description: The LBC1936 is a longitudinal study of healthy ageing, with a focus on cognitive ageing. The sample of 1091 relatively healthy, community-dwelling individuals was recruited between 2004 and 2007. Recruitment and testing are fully described elsewhere,5 and a recent cohort profile article6 describes the data that have been collected to date. They were all born in 1936. Most took part in the Scottish Mental Survey 1947 (SMS1947) which took place on 4th June 1947 and applied the Moray House Test No. 12 (MHT) to almost everyone born in 1936 (~95% of the population; N = 70,805). The SMS1947 was conducted by the Scottish Council for Research in Education, who permitted access to the childhood intelligence data. For the present study, only the childhood MHT scores are used. These were available for 947 subjects, whose mean (SD) age was 10.9 years (0.28) when they sat the test.The same MHT was applied to this sample as was described for the LBC1932/SMS1932. Concurrent validity was confirmed by testing over 1000 children on the Terman-Merrill Revision (Form L) of the Binet Test10. The MHT-Binet correlation was 0.81 for both the boys and the girls.

Quality controls: Genotyping was performed with the Illumina Human610_Quadv1 chip at the Wellcome Trust Clinical Research Facility, Edinburgh, UK. The data were then subjected to the following quality control measures, which have been described previously9. Individuals were excluded based on unresolved gender discrepancy, relatedness, call rate (≤ 0.95), and evidence of non-Caucasian descent. SNPs were included if they met the following conditions: call rate ≥ 0.98, minor allele frequency ≥ 0.01, and Hardy-Weinberg equilibrium test with P ≥ 0.001.

Statistical analysis/additional information: Imputation was performed using the MACH software3 and the CEU reference panel (HAPMAP II rel.23, build 36). Association between the imputed SNPs and childhood intelligence was analysed using dosage scores in an additive model using the MACH2QTL software (V1.0.4)3.

Acknowledgments: See LBC1921.

Brisbane Adolescent Twins Study, Queensland Institute of Medical Research (QIMR) cohort​

Cohort description: The Brisbane Adolescent Twin Study cohort11 is a population sample that supports ongoing studies conducted at the Genetic Epidemiology Laboratory, Queensland Institute of Medical Research (QIMR), Brisbane, on a wide range of traits. IQ data were collected as part of the cognition project12, which targets twins aged 16 years and their siblings and were available for 1752 individuals (778 families), with a mean age of 16.5 years (±1.0 years, range 15.4-28.9 years). Exclusion criteria were parental or self-report of head injury, neurological or psychiatric illness, substance abuse/dependence, or current use of psychoactive medication in either twin. Written, informed consent was obtained from all participants and from a parent or guardian for those aged under 18 years. Ethics approval was obtained from the Human Research Ethics Committee at QIMR.

Intelligence measure: Full-scale IQ in the QIMR cohort was measured using a shortened version of the computerised Multi-dimensional Aptitude Battery (MAB)13, a general intelligence test similar to Wechsler Adult Intelligence Scale-Revised. The shortened MAB includes three verbal subtests (information, arithmetic, vocabulary) and two performance subtests (spatial, object assembly). Scaled scores for full-scale IQ were computed in accordance with the manual.

Quality controls: We applied stringent quality controls as described in Medland et al (2009)14. In particular we removed SNPs based on missingness (Call Rate < 0.95), minor allele frequency (MAF < 1%), Hardy-Weinberg test (HWE P-value < 10-6), Mendelian errors and the mean value of BeadStudio GeneCall score for Illumina array (GeneCall < 70%). We also excluded subjects of Non-European Ancestry based on principal component analysis.

Statistical analysis/additional information: We imputed unobserved genotypes from the HAPMAP II CEU panel (Release 22, NCBI Build36, dbSNP 126) data using MACH4 software. We performed association analysis between SNPs and childhood intelligence under an additive model using a family-based test in MERLIN15.

Acknowledgments: We thank the families who participated; Marlene Grace and Ann Eldridge for sample collection; Kerrie McAloney for study co-ordination; Harry Beeby, Daniel Park, and David Smyth for database support; Anjali Henders for DNA processing and preparation; and Scott Gordon for quality control and management of the genotypes. The cognition project is supported by the Australian Research Council (A79600334, A79906588, A79801419, DP0212016, DP0664638, DP1093900). Genotyping was supported by the National Health and Medical Research Council (389875).

Western Australian Pregnancy Cohort (Raine) Study​

Cohort description: The Raine study is a prospective pregnancy cohort study of 2,868 live births. Women were recruited between May 1989 and November 1991 (N=2,900) through the public antenatal clinic at King Edward Memorial Hospital (KEMH) and nearby private clinics in Perth, Western Australia. Comprehensive data regarding social and demographic characteristics were collected at 18 and at 34 weeks gestation. Data were collected at birth, including physiological and clinical information, and the study children and their families provided sociodemographic and behavioural data at one, two, three, five, eight, ten, 14 and 17 years of age. Complete details of enrolment methods have been published elsewhere16. The Human Ethics Committees at KEMH and/or Princess Margaret Hospital for Children approved the protocols for the study

Intelligence measure: General cognitive ability (‘g factor’) was estimated based on four cognitive measures carried out at approximately 10 years of age (Peabody Picture Vocabulary Test17, Raven’s Colored Progressive Matrices18, Symbol Digits Modalities Test (SDMT)19 written score and SDMT oral score. Principal component analysis was performed using each of the four cognitive measures and the first principal component was used for analyses.

Quality controls: Genotyping was carried out using the Illumina Human660W Quad Array in 1593 children. Individuals were excluded on the basis of gender mismatches (N=7), relatedness (for pairs of individuals with π > 0.1875 the individual with the higher proportion of missing data was excluded; N=63), low genotyping success (>3% missingness; N=16), and heterozygosity (<0.30; N=4). SNPs with minor allele frequency of <1%, a call rate of <95% or Hardy-Weinberg equilibrium violations (p-values <5.7x10-7) were excluded.

Statistical analysis/additional information: Imputation of genotypes was carried out using the CEU samples from Hapmap (Phase 2, Build 36, Release 22) and MACH software (v1.0.16). Association analysis was performed under an additive model using Mach2QTL software.

Acknowledgments: The authors thank the Raine Study participants and their families for their contribution in this study. The authors gratefully acknowledge the NHMRC for their long term contribution to funding the study over the last 20 years and also the following Institutions for providing funding for Core Management of the Raine Study: The University of Western Australia (UWA) Raine Medical Research Foundation UWA, Faculty of Medicine, Dentistry and Health Sciences, The Telethon Institute for Child Health Research Women and Infants Research Foundation and Curtin University. The authors gratefully acknowledge the assistance of the Western Australian DNA Bank (National Health and Medical Research Council of Australia National Enabling Facility). The authors also acknowledge the support of the National Health and Medical Research Council of Australia (Grant ID 572613 and ID 211912) and the Canadian Institutes of Health Research (Grant ID 166067). MJB funded by a Sir Henry Wellcome Fellowship (WT085515).
 
Oh. Hailee.



Yes...

View attachment 908287

*In addition to the standard quality controls, for the TEDS cohort we removed SNPs if the info statistic (IMPUTE2 imputation package) in TEDS and WTCC2 controls < 0.98 (for SNPs that were imputed from HapMap) and < 0.90 (for SNPs that were imputed from HapMap and WTCC2 controls). We removed 927,192 SNPs following this exclusion.

Supplementary Table 2. The effect size of the top 100 SNPs (discovery + replication cohorts) sorted based on the association P-value. The direction was ordered as QIMR, ALSPAC, LBC21, LBC36, RAINE, TEDS, NTR, GenR, and UMN. 0 indicates that the effect size is zero.​

I'm too literaturepilled to understand this :feelshehe:
 
Fuck having a oneitis
 
That is a lot of coom, probably got gangbanged
 
Apologies to anyone offended, if incel and male.

I see now:

1697658250365

1697658258618


1697658265588

1697658272410
 
1698285903326

1698285819194

1698285828742

1698286088068


...

1698285889956

1698285855693

1698285929515

1698285962305

1698285992269

1698286053882

1698286067841

1698286114107

1698286364311
 
Last edited:
My oneitis rn:

zoosextube.life.2.jpg
 
1698333334180


...

A rare exchange between races in America.
 
Im not literally worthless, so I don't have a Oneitis.
 
I don't think about it because a foid that's not mine getting fucked by other men has nothing to do with me
 

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