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      "body": "Epigenetics and MAOA in the brain \nEpigenetics is revolutionizing how scientists think about genetics. Epigenetics refers to external changes to DNA that turn genes “on” or “off” without altering the DNA sequence [26]. Gene expression — the manifestation of genetic potential — is modified in epigenetic processes, even though the gene itself stays intact. The field of epigenetics is largely theoretical, at least insofar as humans are concerned. But growing evidence suggests that epigenetic changes can, in some cases, be passed on from parents to children. They are handed down not as inherited traits, but as non-hereditary modifications transmitted to offspring along with genes from their parents [26].\nVarious environmental factors are thought to influence epigenetic processes. Could epigenetics modify behavioral traits by acting on MAOA gene activity? Scientists are just beginning to understand the effects of MAOA variants on the brain. The low-expression MAOA-3R variant has been linked with a heightened response from the amygdala, a structure in the brain that regulates emotion [27]. 3R is also associated with decreased activity in prefrontal regions of the brain that protect against anxiety [27].\nElena Shumay of the Brookhaven National Laboratory and her team conducted a study to determine how MAOA variants affect brain levels of the MAOA enzyme in healthy men [28]. Using PET imaging scans, these researchers found no correlation between MAOA brain levels and MAOA gene variants. Shumay and her colleagues reasoned that MAOA levels must be regulated by the same region of the MAOA gene where the 2R, 3R, 4R, or other repeat sequence are located. The evidence supported their prediction: it appears that MAOA expression associated with MAOA brain levels is under the control of epigenetic mechanisms [28].\nIn other words, epigenetics may influence whether a tendency toward higher or lower MAOA genetic activity actually manifests itself. The amount of genetic activity, in turn, determines whether there is a larger or smaller quantity of the MAOA enzyme in the brain, which is needed to break down certain neurotransmitters [28].\n \nThere are limits to studying the role of a single gene in antisocial behavior outside of its environmental context. Even when a gene correlates closely with violence or criminal acts, it does not mean that the gene itself codes for aggressive tendencies. According to Kevin Beaver and University of California at Davis’ Jay Belsky, plasticity genes seem to affect how much or how little male youth are influenced by their parents. Beaver and Belsky claim these genes appear to increase susceptibility to environmental effects, “for better and for worse” [29]. Supportive and unsupportive parents are more likely to have a positive or negative impact, respectively, on their children if their kids carry plasticity genes [29].\nYet plasticity genes appear to have a cumulative effect.",
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      "body": "Other 15-point claims\n\nHerrnstein and Murray cite numerous other studies in their book that produce a broad range of estimates for the black/white IQ gap. These range from no gap to a gap of 30 points (an absurd finding on its face, since this would mean that blacks are mentally retarded).\n\nTo put everything in perspective, the authors provide a chart summarizing the findings of 156 studies. (7) The results form a bell curve of their own: the vast majority of studies have found a difference of about 15 points, while only a few studies have found significantly smaller or greater differences. From this chart, one might reasonably conclude that the gap is 15 points.\n\nBut a closer look at the chart reveals some disturbing facts. It was compiled in large part by Arthur Jensen, Frank McGurk, R. Travis Osborne and Audrey Shuey -- all recipients of grants from the Pioneer Fund. This is the neo-Nazi organization that advocates eugenic policies -- namely, the phasing out of black people. This alone does not refute the chart, of course, but one would feel more comfortable with its objectivity if its compilers weren't funded by overt racists.\n\nAnd a look at the footnotes reveals that these fears are well-founded. To be included in the chart, a study had to meet \"basic requirements of interpretability.\" These requirements included several that many would view as fair: for example, that the studies had to include both a black and a white sample, that the sample sizes had to be larger than 50 for each group, etc. But the authors then report that socioeconomic status posed \"a special problem\" for them. They write:\n\n\"If a study explicitly matched subjects by SES, it was excluded. If it simply drew its samples from a low-SES area, it was included, even though some degree of matching had occurred.\" (8)\n\nIt is well-known that matching blacks and whites for socioeconomic status will see a large reduction in the IQ gap. Researchers justifiably dispense with such matching if they want to learn the raw differences. But including samples from \"low-SES areas\" creates great potential for mischief. Inner city schools are disproportionately filled with poor black children, but relatively richer whites are bussed into their schools, where they take the same IQ tests. Furthermore, an IQ test given to a broad region like a city would include inner-city black children and suburban white children. Both study samples would yield unnaturally large IQ gaps.\n\nThe only way to minimize statistical errors (and deception) is to consider nationally representative samples. As our first chart indicates, such tests indicate a 7 to 10-point gap. For those who accept academic achievement tests as valid proxies for IQ tests, the gap in 1990 was about 10 points, after having been reduced about 2.5 points per decade since 1970. (9)\n1. K.R. Vincent, \"Black/white IQ differences: Does age make a difference?\" Journal of Clinical Psychology 47, 1991, pp. 266-270.\n\n2. Richard Herrnstein and Charles Murray, The Bell Curve, (New York: Simon & Schuster, 1994), pp. 289-90.\n\n3. Marilyn Elias, \"Experts find fault with 'Bell Curve'\" USA Today. (No date given; probably Fall 1995.)\n\n4. Richard Nisbett, \"Race, IQ and Scientism,\" pp. 50-52 in Steven Fraser, ed., The Bell Curve Wars (New York: HarperCollins, 1995).\n\n5. Herrnstein and Murray, p. 356.\n\n6. Ibid., p. 355.\n\n7. Ibid., pp. 276-77.\n\n8. Ibid., p. 717.\n\n9. Nisbett, p. 49. The academic tests used for this statistic are listed in the chart below, which has been compiled from his written account:\nPoint reduction in black/white IQ gap (1970-1990)*\n\nTest                                         Reduction\n------------------------------------------------------\nNational Assessment of Education Progress    4.2 points\nScholastic Aptitude Test                     5.0\nNational High School Studies                 4.5\nAmerican College Test                        4.4\nGraduate Record Examination                  5.7\n\n*Total reductions have been extrapolated from different-length\nstudies to represent two decade period. Original lengths: NAEP,\n1970-1990; SAT, 1976-1993; NHSS, 1973-1982; ACT, 1980-1991; GRE,\n1980-1988.\n\n\n\nImpulsivity\n\nHere was a study that linked thrill seeking and impulsivity together and tried to find a correlation with an impulsive behaviour (like drinking).\nRacial differences in disinhibition have been little studied, and available findings present a complex picture. Importantly, in a review of racial differences in risk factors for adolescent drinking and drug use, Wallace and Muroff (2002) omitted any discussion of disinhibition. Cross-sectional research suggests that European American youth have higher levels of sensation seeking than African American youth (e.g., Hoyle, Stephenson, Palmgreen, Lorch, & Donohew, 2002; Russo, Stokes, Lahey, Christ, McBurnett, Loeber, Stouthamer-Loeber, & Green, 1993). Similarly, Crawford and colleagues (2003) found that European American children had higher levels of and sharper increases in sensation seeking than other ethnicities over a two-year period in middle school.\nResearch also suggests that sensation seeking may relate more strongly to risky behaviors among European Americans than among African Americans. For example, Cooper and colleagues (2003) found sensation seeking related to a general factor of problem behavior (i.e., risky sexual activity, substance use, delinquency, academic underachievement) for European American but not for African American adolescents. Additionally, a meta-analysis (Hittner & Swickert, 2006) found that sensation seeking related more strongly to alcohol use in studies having a higher percentage of European Americans, suggesting that sensation seeking may relate more strongly to alcohol use for this racial group.\n \nConsistent with having higher levels of sensation seeking, European American adolescents also drank alcohol more frequently than African American youth in this sample. Importantly, the higher initial levels of sensation seeking were found to at least partially account for the higher level of alcohol use for European Americans. Additionally, we found tentative support that change in sensation seeking from childhood into adolescence is related to increased alcohol use frequency for European Americans but not for African Americans. This finding is consistent with a meta-analysis (Hittner & Swickert, 2006) that showed sensation seeking was more strongly related to alcohol use in samples with a higher proportion of European Americans. There are several potential reasons why this association is not found (or is less strong) in African American youth. For example, having deviant or substance-using peers has been shown to at least partially explain the association between sensation seeking and alcohol/drug use (Yanovitzky, 2005). However, African American youth are more likely than European American youth to have close friends who disapprove of alcohol use (e.g., Herd, 1997) which could attenuate this association. Future research incorporating culture-specific factors (e.g., discrimination, religiosity, peer use) that may constrain the association between sensation seeking and alcohol use for African Americans is needed (e.g., Gibbons et al., 2007; Michalak, Trocki, & Bond, 2007).\none potential contributor may be socioeconomic status (SES). Lower SES is related to higher levels of impulsivity.\nEven controlling for socio-economic status, blacks still gain less at a higher SES, and many black families still reside in poor neighbourhoods despite not being poor, which still puts them at a disadvantage.\nhttps://mathcs.clarku.edu/huxley/UnColl/Rdetc/NegPl.html\n \nThe fact that they need to be persuaded would imply that they are less impulsive.. Also why are all your sources from 1853? Did you expect these to be unbiased?\nAnother study:\n“In the overall sample, higher household income (b = −0.01, 95% CI = −0.01 to 0.00) and maternal education (b = −0.24, 95% CI = −0.44 to −0.04) at birth were associated with lower youth impulsivity at age 15, independent of race, gender, and family structure. A significant interaction was found between race and household income at birth (b = 0.01, 95% CI = 0.00 to 0.02) on subsequent youth impulsivity, which was indicative of a stronger protective effect for Whites compared to Blacks. Blacks’ diminished return exists for the long-term protective effects of family income at birth against subsequent youth impulsivity. The relative disadvantage of Blacks in comparison to Whites is in line with a growing literature showing that Black families gain less from high SES, which is possibly due to the existing structural racism in the US.”\nSeveral links between sensation seeking and aggression have been found:\nhttps://www.ncbi.nlm.nih.gov/pubmed/20973087\nhttps://www.frontiersin.org/articles/10.3389/fpsyg.2016.01447/full\n \nWhites are also considerably more likely to get stressed than blacks. There have been links with stress and aggression.\nhttps://www.oxfordscholarship.com/view/10.1093/acprof:oso/9780195168761.001.0001/acprof-9780195168761-chapter-12\nChild impulsivity was measured during the first six annual assessments using an abridged version of the Eysenck Impulsivity Scale (Eysenck, Easting, & Pearson, 1984). Children (8 items) and mothers (13 items) reported about the child’s impulsivity (e.g., Does the child “generally say things without stopping to think?”; 1 = no, 2 = yes). For each assessment, scores were averaged across items for each reporter (higher scores = greater impulsivity). Mother- and child-reported impulsivity were analyzed separately due to their low correlations (r’s ranged from .21 to .36, p’s < .0001). This level of correlation is consistent with a large body of research (Achenbach, McConaughy, & Howell, 1987). Across assessments the average alpha for impulsivity for African Americans (mother-report: α = .87, inter-item correlation = .34; child-report: α = .68, inter-item correlation = .22) and European Americans (mother-report: α = .86, inter-item correlation = .33; child-report: α = .72, inter-item correlation = .25) was acceptable.\n\n Results for impulsivity showed a different pattern: African Americans had higher initial levels of impulsivity than European Americans (mother-reported: β = −0.16, p < .01; child-reported: β = −0.27, p < .001; see Figure 2) but rates of change did not differ by race. LGCMs were re-run adding parental occupational status to more stringently examine if differences in SES could account for these results. (AKA, white children and black children are impulsive at thr same rate.)\n\nSexual activity\n\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767847/\n\nhttps://www.npr.org/templates/story/story.php?storyId=114237523\n\nhttps://www.latimes.com/local/california/la-me-ln-std-stigma-20180507-htmlstory.html\n\nhttps://en.wikipedia.org/wiki/Polygamy_in_Christianity#Exceptions_in_Africa\n\nhttps://jamanetwork.com/journals/jamapediatrics/fullarticle/350980\nIs systemic racism to blame?\nLos Angeles County launched a Center for Health Equity in October to address the idea that “health predominantly happens outside the health care setting,” said its director, Heather Jue Northover, at a recent meeting. “It happens where we live, work, play and pray.”\nThe center will target five health disparities, including high rates of STDs among certain minority groups.\nNationwide, STD rates have been climbing for the past five years. More people were diagnosed with syphilis, chlamydia or gonorrhea in 2016 than ever before.\nSome blame underfunding of STD prevention programs, as well as falling condom usage. There’s also speculation that people are having sex with more partners because of hookup apps.\nBut the picture is more complicated when it comes to the high STD rates among minorities. Gay and bisexual men make up the vast majority of new syphilis cases. In L.A. County, syphilis rates among African American women are six times higher than white women and three times higher than Latina women.\nNorthover said that officials need to evaluate what’s called structural or systemic racism, the way housing or education policies may negatively impact people and their health. Studies have found, for example, that people with HIV who had low levels of literacy were less likely to follow their treatment, and that poorer Americans were more likely to engage in risky sexual behavior, increasing their risk of STDs.\nThe Centers for Disease Control and Prevention released a white paper in 2010 saying the country could not close disparities in STD rates without addressing “the interpersonal, network, community, and societal influences of disease transmission and health.”\nBut that’s a tall order given how entrenched many social problems are.\nPoverty or a lack of opportunity may be forcing women to exchange sex for resources, leading to the spread of STDs, Northover said. There also tends to be a mistrust of the medical system among African Americans, making them reluctant to seek care. Certain neighborhoods may be excluded from access to healthcare because of geography or finances, she said.\n“We need to take a wider lens,” said Northover, who added that she’s still trying to get to the bottom of what’s driving STD rates.\nCounty Supervisor Mark Ridley-Thomas, who represents South Los Angeles, convened several community groups in 2012 to try to bring down STD rates through collaboration. But the still-growing case numbers suggest the approach needs to be reimagined, said Dr. Michael Hochman, a senior health deputy for the supervisor.\n“If you keep doing the same thing and expect a different result, then that’s insanity,” Hochman said.\nGenes/alleles\nMAOA is not the only gene that affects violent behavior, Reif et al found that the short allele of 5-HTTLPR enhanced the aggression effect of the 3-repeat allele of MAOA. Reif et al did not find a “main effect” of 5-HTTLPR alone on aggression, but a few other studies have. In the case of MAOA, the 3-repeat allele is much more common in Africans and Asians than in whites, but for 5-HTTLPR, the short allele is found in about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans. In truth, Retz determined that the short allele only increased violence 5%. Plus, Patkar et al failed to find an effect of the short allele on aggression in African Americans, suggesting that the gene could have different effects in different races. \nThey also argued for the importance of teaching people not to overgeneralize or stereotype individuals based on average group differences, because of the significant overlap of people with varying intelligence between different races.[99]\nThe MAOA-L allele test was never conducted on pure Africans.\nhttps://geneticliteracyproject.org/2014/10/29/genes-linked-to-violent-crime-but-can-they-explain-criminal-behavior/\nThe 2009 study by McDermott and four colleagues, \"Monoamine Oxidase A Gene (MAOA) Predicts Behavioral Aggression Following Provocation,\" which triggered much of the recent publicity given to the warrior gene, was published in Proceedings of the National Academy of Sciences (PNAS). The article claimed that MAOA-L carriers were more likely than noncarriers to respond with \"behavioral aggression\" toward someone they thought had cheated them out of money they had earned in a laboratory test. \"Behavioral aggression\" was defined as making the putative cheater consume hot sauce.\n \nEven disregarding the issue of whether giving someone hot sauce counts as \"physical aggression,\" McDermott's study provides little to no evidence for the warrior gene, because the difference between carriers and noncarriers was minuscule. McDermott et al. examined 70 subjects, half of whom carried the warrior gene. The researchers found that 75 percent of the warrior gene carriers \"meted out aggression\" when cheated—but so did 62 percent of the noncarriers. Moreover, when subjects were cheated out of smaller amounts of money, \"there was no difference\" between the two groups.\nhttps://www.news.com.au/world/breaking-news/scientists-debunk-maori-warrior-gene-myth/news-story/117e673dd450b9b002d961e39fabc1b6\nhttps://www.mygenefood.com/warrior-gene-5-common-myths/\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058761/",
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      "body": "than that for Mexican-American and non-Hispanic white children, indicating that differences in risk for exposure still persist.\"[75]\nEnvironmental factors including childhood lead exposure,[74] low rates of breast feeding,[76] and poor nutrition[77][78] can significantly affect cognitive development and functioning. For example, childhood exposure to lead, associated with homes in poorer areas[79] causes an average IQ drop of 7 points,[80] and iodine deficiency causes a fall, on average, of 12 IQ points.[81][82] Such impairments may sometimes be permanent, sometimes be partially or wholly compensated for by later growth. The first two years of life is the critical time for malnutrition, the consequences of which are often irreversible and include poor cognitive development, educability, and future economic productivity.[83] The African American population of the United States is statistically more likely to be exposed to many detrimental environmental factors such as poorer neighborhoods, schools, nutrition, and prenatal and postnatal health care.[84][85] Mackintosh points out that for American blacks infant mortality is about twice as high as for whites, and low birthweight is twice as prevalent. At the same time white mothers are twice as likely to breastfeed their infants, and breastfeeding is highly correlated with IQ for low birthweight infants. In this way a wide number of health related factors that influence IQ are unequally distributed between the two groups.[86]\nThe Copenhagen consensus in 2004 stated that lack of both iodine and iron has been implicated in impaired brain development, and this can affect enormous numbers of people: it is estimated that one-third of the total global population are affected by iodine deficiency. In developing countries, it is estimated that 40% of children aged four and under suffer from anaemia because of insufficient iron in their diets.[87]\nOther scholars have found that simply the standard of nutrition has a significant effect on population intelligence, and that the Flynn effect may be caused by increasing nutrition standards across the world.[88] James Flynn has himself argued against this view.[89]\nSome recent research has argued that the retardation caused in brain development by infectious diseases, many of which are more prevalent in non-white populations, may be an important factor in explaining the differences in IQ between different regions of the world.[90] The findings of this research, showing the correlation between IQ, race and infectious diseases was also shown to apply to the IQ gap in the US, suggesting that this may be an important environmental factor.[91]\n\nEarl Hunt states that brain size is found to have a correlation of about .35 with intelligence among whites and cites studies showing that genes may account for as much as 90% of individual variation in brain size. According to Hunt, race differences in average brain size could potentially be an important argument for a possible genetic contribution to racial IQ gaps. Nonetheless, Hunt notes that Rushton's head size data would account for a difference of .09 standard deviations between black and white average test scores, less than a tenth of the 1.0 standard deviation gap in average scores that is observed.[154][189] Wicherts, Borsboom, & Dolan (2010) argue that black-white differences in brain size are insufficient to explain 91% to 95% of the black-white IQ gap.[190]\nArchaeological data\nArchaeological evidence does not support claims by Rushton and others that blacks' cognitive ability was inferior to whites' during prehistoric times as a result of evolution.[191]\n\nAnd the argument that hanging around people with low-IQ will reduce quality of life is.. Dumb, because a) that would mean that the black person hanging around you would also have a high IQ, b) hanging around “dumb” people shouldn’t make you dumber, and c) is high IQ associated with high quality of life, or is high quality of life associated with high IQ? It’s been proven that socio-economic status affects IQ, not the other way around.\n\nhttps://www.motherjones.com/kevin-drum/2019/06/heres-why-the-black-white-iq-gap-is-almost-certainly-environmental/\n\nThere’s a famous result in intelligence studies called the Flynn Effect. What it tells us is that average IQs rose about 3 points per decade throughout the 20th century. That’s roughly 20 points of IQ throughout the entire period, and it’s obvious that this couldn’t have been caused by genes.³ It’s 100 percent environmental. This is clear evidence that environmental factors are quite powerful and can easily account for very large IQ differences over a very short period of time.\nThe difference in average IQ recorded in different European countries is large: on the order of 10 points or more. The genetic background of all these countries is nearly identical, which means, again, that something related to culture, environment, and education is having a large effect.\nIt is very common for marginalized groups to have low IQs. In the early years of the 20th century, for example, the recorded IQs of Italian-Americans, Irish-Americans, Polish-Americans and so forth were very low. This was the case even for IQ scores recorded from the children of immigrants, all of whom were born and educated in the US and were fluent English speakers. These IQ scores weren’t low because of test discrimination (at least not primarily because of that), they were low because marginalized groups often internalize the idea that they aren’t intelligent. However, over the decades, as these groups became accepted as “white,” their IQ scores rose to the average for white Americans.\nThe same thing has happened elsewhere. In the middle part of the 20th century, the Irish famously had average IQ scores that were similar to those of American blacks—despite the fact that they’re genetically barely distinguishable from the British. However, as Ireland became richer and the Irish themselves became less marginalized, their IQ scores rose. Today their scores are pretty average.\nIn 1959, Klaus Eyferth performed a study of children in Germany whose fathers had been part of the occupation forces. Some had white fathers and some had black fathers. The IQ scores of the white children and the racially mixed children was virtually identical.\nOver the past few decades, the black-white IQ gap has narrowed. Roughly speaking, it was about 15 points in 1970 and it’s about 10 points now. This obviously has nothing to do with genes.\n \n\n\nCurrently, the 1.1 standard deviation difference in average IQ between Blacks and Whites in the United States is not in itself a matter of empirical dispute. A meta-analytic review by Roth, Bevier, Bobko, Switzer, and Tyler (2001) showed it also holds for college and university application tests such as the Scholastic Aptitude Test (SAT; N  2.4 million) and the Graduate Record Examination (GRE; N  2.3 million), as well as for tests for job applicants in corporate settings (N  0.5 million) and in the military (N  0.4 million). Because test scores are the best predictor of economic success in Western society (Schmidt & Hunter, 1998), these group differences have important societal outcomes (R. A. Gordon, 1997; Gottfredson, 1997). The question that still remains is whether the cause of group differences in average IQ is purely social, economic, and cultural or whether genetic factors are also involved. Following publication of The Bell Curve, the American Psychological Association (APA) established an 11-person Task Force (Neisser et al., 1996) to evaluate the book’s conclusions. Based on their review of twin and other kinship studies, the Task Force for the most part agreed with Jensen’s (1969) Harvard Educational Review article and The Bell Curve, that within the White population the heritability of IQ is “around .75” (p. 85). As to the cause of the mean Black–White group difference, however, the Task Force concluded: “There is certainly no support for a genetic interpretation” (p. 97)\n\n\nhttps://www.forbes.com/sites/quora/2019/08/14/statistics-show-iq-disparities-between-races-heres-what-that-really-means/#5e17cc4c4490\n\nAmong scientists, it has been common knowledge that both black and white IQs have been rising over the decades, with black IQs converging upwards towards whites. This fits nicely with America's rising standard of living, which has been rising somewhat faster for blacks, thanks to the Civil Rights movement and other anti-poverty measures.\n\nThe authors of The Bell Curve, then, face an uphill battle in trying to prove that black and white IQs are not converging, but diverging. They attribute this divergence to \"dysgenesis,\" which supposedly results when dull people interbreed. In fact, they assert this downward trend in spite of the famous \"Flynn Effect,\" which has been raising IQs for all people and all classes world-wide, about 3 points per decade.\n\nIn a second departure from scientific consensus, the authors also maintain that the IQ gap between blacks and whites is 15 points, an usually high figure. But this is not what four major IQ tests for children have found:\nBlack/white IQ gap in major IQ tests (1991) (1)\n\nRavens Standard Progressive Matrices       7 points\nKaufman Assessment Battery for Children    7\nStanford-Binet IV (two separate studies)  10\nThe authors of The Bell Curve note these numbers, but dismiss them. The Kaufman-ABC results, they claim, suffer from statistical problems. (2) Even granting them their objection, however, still leaves three major studies showing a 7 to 10-point gap, not a 15-point one.\n\nWhy do the authors discount both the Flynn Effect and these test results in their assessment of black IQ? Because of a single study: their analysis of the National Longitudinal Survey of Youth (NLSY). The NLSY has tracked the lives of 12,000 young people since 1979, at one point giving them an Armed Forces Qualification Test (AFQT). But The Bell Curve's analysis of the NLSY data is deeply flawed. First of all, the AFQT isn't even an IQ test. \"This is an achievement test,\" said Halford Fairchild of the American Psychological Association said, in its authoritative review of The Bell Curve. \"It shows the extent to which you've benefited from school. To assert it's a proxy for IQ is a big lie.\" (3)\n\nEven if we accept the AFQT as an IQ test, however, the authors still commit serious errors analyzing it. One of the best-known critics of their methodology is psychologist Richard Nisbett, whose arguments follow here. (4) Herrnstein and Murray's comparison of black and white IQs did not follow the changing IQs of children over a period of time (the most reliable method), but differences of IQ between mothers and children at a fixed point in time (which introduces all sorts of statistical complications). Herrnstein and Murray found that the black/white IQ gap among mothers was 13.2 points, but among their children was 17.5 points. (5) This four-point increase forms the basis of their claim that the black/white IQ gap is growing.\n\nHowever, the study itself is unrepresentative of the nation at large; the average IQ of the children was 92, significantly below the national average of 100. The reason is because the women in this long-term survey had not finished their childbearing years, so all the children in the study had been born to young mothers. Unfortunately, young motherhood is correlated to low IQ, which is why their children scored so far below the national average.\n\nHerrnstein and Murray note this problem, and claim that sampling weights added to the NLSY make the survey sample \"nationally representative.\" (6) But this leads to trouble when they attempt to analyze a growing IQ gap in children. Young motherhood is not unusual for black women, but for white mothers it suggests low socioeconomic status, which in turn suggests low IQ. Therefore, the IQs of the young white and black mothers were similar… although the IQs of their children were bound to diverge. Why? Because black mothers, having average black IQs, would have children with the same. But white mothers, with below-average white IQs, would have children with IQs that would tend to rebound back towards the higher white average. That's because trait variation is natural in children, and if white parents are already near the bottom, then their children, if they vary, have nowhere else to go but up. This is technically known as \"regression towards the mean,\" and it is a common statistical deception. You can get the opposite \"result\" by comparing average black mothers with the smartest white mothers; the white children would tend to drop back down to the white average, having nowhere else to go but down. In this case, Herrnstein and Murray could have reported that IQ gap is shrinking, not growing!\n\nThanks to this statistical anomaly, Herrnstein and Murray found a four-point increase in the black/white IQ gap in their particular sample. On this basis, they then argued that the gap is growing everywhere. But this is certainly not the case, and the mainstream studies remain the best indicator of the shrinking black/white IQ gap.",
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      "body": "For the “pecularities of the negro brain”, read this: \n-Paul Brocca- -Manipulated Data and hypothesis about posterior placement of foramen magnum to support white superiority\n-Didn’t account for uncontrolled factors of brains\n-used the location of the foranen magnum as a divider of genu and splenium to conclude that\nwhites were better\n\nhttps://neurophilosophy.wordpress.com/2007/03/14/on-the-peculiarities-of-the-negro-brain/\n\nhttps://www.nola.com/news/politics/article_7f4c11a5-459f-557a-9f58-39907433a8e6.html\n\nIf one is “concerned simply with the question whether [human races]… are different”, then “there can be no doubt as to the answer”. However, “the words 'superior’ and 'inferior’ are not generally used unless value judgements are concerned” (p421).\n\nAny value judgement is necessarily subjective. On objective criteria, each group can only be demonstrated to be, on average, superior in a specific endeavour (e.g. IQ tests, sports, mugging, tanning, building civilizations). The value ascribed to these endeavours is, however, wholly subjective.\n\nContemporary hereditarians therefore disclaim any association between their theories and notions of racial supremacy. However, these hereditarians are the same individuals who emphasise the predictive power of IQ tests in determining many social outcomes which are generally viewed in anything but value-neutral terms (e.g. wealth, criminality, illegitimacy, welfare dependency: see The Bell Curve).\n\nFrom a biological perspective, no species (or subspecies) is superior to another. Each is equally adapted to its own ecological niche.\n\n\n\namygdala, hippocampus, lateral ventricles, caudate nucleus, orbitofrontal cortex (OFC) and total cerebrum. Each participant completed a 1.5 T magnetic resonance imaging (MRI). Our primary finding in analyses of brain subregions was that when compared to Caucasians, African Americans exhibited larger left OFC volumes (F 1,68 = 7.50, p = 0.008).\n\n[...] there were no statistically significant differences in total gray matter, total white matter, or ventricular CSF volumes. In models examining specific brain regions, the only statistically significant difference was that African-Americans exhibited larger left OFC volumes than Caucasians. However, when regional ratios were examined (regional volume/total cerebral volume), the African-American cohort exhibited greater ratios for the right amygdala and bilaterally for the OFC\n\n\n\n\nIQ DIFFERENCES\n\nAfrican IQs vs. American Black IQs\nThe estimate of Africa IQ being on average 2 SD below is based on Lynn's cherry-picked data. A systematic review showed that Lynn artificially reduced the average by at least 12 points. Countries like Swaziland even have a higher national IQ than American blacks with zero European mixture. Also the BW gap in the US has been reduced by .33 SD to around 9. Toxic lead exposure in childhood can reduce IQs by 6 points and black children have 50 percent higher blood-lead content on average due to the environmental effects of housing segregation. Known social and environmental factors can account for most if not all the gap.\nhttps://jeltewichertsdotnet…\n\nhttp://www.apa.org/pubs/jou…\n\nNo study to date has shown a correlation between levels of European admixture and IQ. Even Rushton and Jensen admit as much:\nRacial admixture studies have clearly failed to support the hereditarian\ninterpretation of the Black–White IQ gap. Instead, they have provided\nevidence that seems to contradict it. Even Rushton and Jensen (2005)\nacknowledged that “blood groups distinguishing African from European\nancestry did not predict IQ scores in Black samples” (p. 262), but on the\nsame page they claimed inexplicably that “studies of racial hybrids are\ngenerally consistent with the genetic hypothesis, [although] to date\nthey are not conclusive”. Nisbett (2005, p. 309) responded to Rushton\nand Jensen with what seems like a more reasonable conclusion: “The\nmost directly relevant research concerns degree of European ancestry\nin the Black population. There is not a shred of evidence in this literature,\nwhich draws on studies having a total of five very different designs,\nthat the gap has a genetic basis.”\nhttps://www2.le.ac.uk/depar…\n\nHealth and Nutrition\nPercentage of children aged 1–5 with blood lead levels at least 10 µg/dL. Black and Hispanic children have much higher levels than white children. A 10 µg/dL increase in blood lead at 24 months is associated with a 5.8-point decline in IQ.[74] Although the Geometric Mean Blood Lead Levels (GM BLL) are declining, a CDC report (2002) states that: \"However, the GM BLL for non-Hispanic black children remains higher",
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      "body": "No race is a different species.\n\nmodern humans;\n(hyo͞o′mən) 1. A member of the species Homo sapiens; a human being. 2. A member of any of the extinct species of the genus Homo, such as Homo erectus or Homo habilis, that are considered ancestral or closely related to modern humans.\n\nNot only are all humans modern humans, but anatomically modern humans, well would you look at that, originated in Africa.\n\n\nTraditionally, subspecies are seen as geographically isolated and genetically differentiated populations. Studies of human genetic variation show that human populations are not geographically isolated, and their genetic differences are far smaller than those among comparable subspecies.\n\nWe, by definition, cannot be classified into different subspecies.\n\n\nArchaic humans went extinct long ago.\n\nAnatomically modern humans appear from over 160,000 years ago in Ethiopia and after 70,000 years ago (see Toba catastrophe theory), gradually supplanting the \"archaic\" human varieties. Non-modern varieties of Homo are certain to have survived until after 30,000 years ago, and perhaps until as recently as 12,000 years ago. Which of these, if any, are included under the term \"archaic human\" is a matter of definition and varies among authors. Nonetheless, according to recent genetic studies, modern humans may have bred with \"at least two groups\" of ancient humans: Neanderthals and Denisovans.[4] Other studies have cast doubt on admixture being the source of the shared genetic markers between archaic and modern humans, pointing to an ancestral origin of the traits which originated 500,000–800,000 years ago.[5][6][7]\n\nALL humans are Homo Sapiens. No one is less archaic than another.\n\n“ A common criterion for recognizing two distinct populations as subspecies rather than full species is the ability of them to interbreed without a fitness penalty”\nSubspecies - Wikipedia\n\nFitness in the evolutionary context means ability to breed.\n\nThus neanderthals were a separate subspecies because male hybrid offspring had fitness issues \n“While Neanderthal males themselves were likely good at breeding, their half-human sons weren't and \"they must have been disappointed in their sons,\" said Nature co-author Svante Paabo of the Max Planck Institute in Germany.”\n\nThe result being no neanderthal influence on the Y chromosome.\n\nWhich is also why the descendants and Africans today are the same subspecies - there is no fitness deficit associated with interbreeding between populations in modern humans.\n\nAgain, by definition, you cannot validly classify the races into different subspecies. If that were the case, then what about eye colour? Height? Weight? Hair colour? Sex would be a more valid classification for different races than ancestry/ethnicity is. Even if one thinks it is valid to agree that there a subspecies of human, in a taxonomic hierarchy, race and subspecies are equal. There is no objective way to measure superiority.\n\n“Even though there is a broad scientific agreement that essentialist and typological conceptualizations of race are untenable, scientists around the world continue to conceptualize race in widely differing ways, some of which have essentialist implications.[10] While some researchers use the concept of race to make distinctions among fuzzy sets of traits or observable differences in behaviour, others in the scientific community suggest that the idea of race often is used in a naive[5] or simplistic way,[11] and argue that, among humans, race has no taxonomic significance by pointing out that all living humans belong to the same species, Homo sapiens, and (as far as applicable) subspecies, Homo sapiens sapiens.[12][13]”\n\n“Estimating our ancestral composition down to 0.1% seem to suggest that there are exact, categorical divisions between human populations. But reality is far less simple. Compared to the general public’s enthusiasm for ancestry testing, the reaction from scientists has been considerably more lukewarm. Research indicates that the concept of “five races” does, to an extent, describe the way human populations are distributed among the continents—but the lines between races are much more blurred than ancestry testing companies would have us believe “\n\nA landmark 2002 study by Stanford scientists examined the question of human diversity by looking at the distribution across seven major geographical regions of 4,000 alleles. Alleles are the different “flavors” of a gene. For instance, all humans have the same genes that code for hair: the different alleles are why hair comes in all types of colors and textures.\n\nIn the Stanford study, over 92% of alleles were found in two or more regions, and almost half of the alleles studied were present in all seven major geographical regions. The observation that the vast majority of the alleles were shared over multiple regions, or even throughout the entire world, points to the fundamental similarity of all people around the world—an idea that has been supported by many other studies (Figure 1B).\n\nIf separate racial or ethnic groups actually existed, we would expect to find “trademark” alleles and other genetic features that are characteristic of a single group but not present in any others. However, the 2002 Stanford study found that only 7.4% of over 4000 alleles were specific to one geographical region. Furthermore, even when region-specific alleles did appear, they only occurred in about 1% of the people from that region—hardly enough to be any kind of trademark. Thus, there is no evidence that the groups we commonly call “races” have distinct, unifying genetic identities. In fact, there is ample variation within races (Figure 1B).\n\nUltimately, there is so much ambiguity between the races, and so much variation within them, that two people of European descent may be more genetically similar to an Asian person than they are to each other (Figure 2).\n\nhttps://www.genome.gov/about-genomics/fact-sheets/Genetics-vs-Genomics\n\nMixed children do not face higher health risks: \n\nMost studies are based on clinical reports or reports of mixed-race samples without comparison to single-race groups. It is not surprising that such samples lead to the conclusion of emotional and behavior problems, as clinical samples are self-selected for problems. No national data on adolescents have been reported, except from the sample we used.\n\n“The most common explanation for the high-risk status is the struggle with identity formation, leading to lack of self-esteem, social isolation, and problems of family dynamics in mixed-race households.1–6 This literature is not entirely consistent. In some studies no differences are found between mixed-race and single-race children.7–9 This article explores the risk status of self-identified mixed-race compared with single-race adolescents using a large, nationally representative sample.”\n\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448064/\n\n\nYou said \"The grey substance of the brain of a Negro is of a darker color than that of the European, that the whole brain is of a smokey tint, and that the pia mater [the innermost membrane covering the brain] contains brown spots, which are never found in the brain of a European.\"\n\nAre you referring to melanin in the brain (neuromelanin)? Because the effects of neuromelanin in the brain are only positive (superior athletic ability, superior learning ability)\n\nSmoking patterns and health consequences have been shown to vary widely between Black and White smokers. For example, smoking prevalence is lower among Blacks (19.8%) than Whites (21.4%),1 Blacks smoke fewer cigarettes per day,2,3 Blacks have reported equal or higher desire to quit smoking.\n\n“The total and nonrenal clearances of nicotine were not significantly different, respectively, in blacks (17.7 and 17.2 mL·min−1·kg−1) compared with whites (19.6 and 18.9 mL·min−1·kg−1) (P=.11 and .20). However, the total and nonrenal clearances of cotinine were significantly lower, respectively, in blacks (0.56 and 0.47 mL·min−1·kg−1) than in whites (0.68 vs 0.61 mL·min−1·kg−1; P =.009 for each comparison). The nicotine intake per cigarette was 30% greater in blacks compared with whites (1.41 vs 1.09 mg per cigarette, respectively; P =.02)”\n\nAlso more blacks smoke menthol cigarettes. Menthol cigarettes are suggested to be more addictive.\n\n“Menthol smokers show significantly higher levels of nicotine addiction compared with non menthol smokers in the same age group. Menthol may help to cover the actual strength of cigarette smoke making it more pleasurable and more difficult to quit.”\n\nWhy group every single member of genetic ancestry together as if averages aren’t just averages but represent every single human being? After all, the genetic variation within groups is far greater than the differences between them.\n\nBRAIN DIFFERENCES\n\n\nAs I said Africa has many population clusters and the greatest genetic diversity. Some separate population clusters even live in different parts of the same country. It's pretty unscientific to group them all together as (Negroid).\nI really think you have a strange concept of how academia works. It's not a matter of people being \"squeamish\" or a taboo about the research. They just kind of feel it would be like trying to disprove gravity.\n\nWhat we know about evolution and how long it takes, doesn't support \"sub-speciation.\" It takes about 1 million years for significant evolutionary change to occur even in extreme isolation. Humans left Africa about 100,000-50,000 years ago, so that is not enough time for significant changes to occur genetically except for the phenotypical adaptations most relevant to environment, i.e. skin color, which is why you have people in equatorial regions of Southeast Asia and Australian aborigines with skin almost as dark as black Africans, but totally different genetics.\nFurthermore, the selection mechanism of evolution obviously started to slow down as societies settled and formed civilizations. For natural selection to occur, poor adaptation to a species environment has to prevent the species from reaching reproductive age. Once settled, most humans were able to reach reproductive age with no problem, so evolution slowed down and largely became a social phenomenon of adapting, not genetically but through forms of social organization and technology.\n3.) The biological definition for race and subspecies is about 17 percent to 25 percent genetic difference. The general consensus among the genetics community is that Genetic difference between *any* given population is less than 10 percent.\nSo as you can see, it's not \"sociology\" or the \"humanities\" that define race as a social construct. It's the hard sciences, i.e. biology and genetics, that take this view. The only dissenters against this consensus are all in the soft sciences (mostly psychology) and the vast majority of them (Jensen, Rushton, Gottfredson, Lynn, MacDonald) are funded by the Pioneer Fund, which got its start collaborating with Nazi eugenicists.\nIf Steve Hsu is the best example of someone in the natural sciences, you can come up with, then you're in trouble. \"But he's a theoretical physicist, so he must be smart, right?\" Yeah, but he also authored a bunch of Bible books and religion and Biology aren't exactly sympatico. Ben Carson is a brain surgeon, but I don't really trust his theories about who built the pyramids and for what purpose.\n\nthe difference is actually marginal when you consider that the amount of variation within groups is about 130 cu. cm. Brain size is very weakly correlated with IQ. In vivo brain size isn't necessarily genetic. The brain is plastic. It's size is not fixed. You can increase the size of your brain by learning to juggle. Environmental factors can affect your brain size like lead exposure in infancy/childhood as well as maternal nutrition. \n\n**Also, Nisbett compared the average black brain size to measurements of Einstein's brain and the average was higher. Furthermore, most research seems to point to intelligence being a function of brain structure not size.**\n\nOne of the studies you cited (the ..) explicitly stated that their physique was poor, and implies that the selected Kenyan might have been malnourished. This was also, only 1 person.",
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      "body": "Alright, time to refute your points:\n\nLet me just start off by saying that one of the many glaring flaws of biological realism implies that the way things are is the way they must be.\n\n\n\nGenetics\n\nSo, the people making that claim have no idea how to read that paper. It doesn't claim that \"black africans are genetically closer to bonobos than to white humans\". The paper isn't an easy read, because I'm not a doctorate in evolutionary biology. The summary seems to be this though...\nThe authors are interested in connecting behavior and genetics in bonobos, humans, and chimps (since they're closely related I assume they think that is a good place to start). They start by saying something along the lines that genetic differences don't seem to fully account for behavioral changes. So, they are trying to further examine possible explanations. The figure of interest doesn't say anything along the lines of what people are claiming it does. The figure of interest essentially says that Africans have (or had) closer gender ratios to those of Bonobo populations than to Europeans. That is, for example, if you took the percent females in European Humans, African Humans, and Bonobos; the percent in African Humans and Bonobos would be more similar - clearly this is not how bigoted people are trying to make it seem. Also, the authors aren't making those claims, its people twisting what the authors are saying beyond the point of recognition.\nIt is possible that my interpretation is flawed (I don't have the time to thoroughly read the whole article), but I can guarantee that the authors are not making the claim that people are putting in their mouths.\nEDIT: IN FACT, the authors include a phylogeny showing humans grouped as one leaf (meaning they're essentially the same genetically) that diverged from a shared ancestor with bonobos at some time in past (approx 4.5mya); which is read as, all humans (regardless of race, ethnicity, etc) are equally related to bonobos. Figure: http://www.nature.com/nature/journal/v486/n7404/fig_tab/nature11128_F3.html\nTLDR: The authors don't claim that Africans are genetically closer to Bonobos than Europeans. Their figure shows that Africans are more similar to Bonobos in one demographic (which they are trying to link to social/behavorial traits among humans, chimps, and bonobos) - no racist claim attempted. One could just as easily say that Africans are more similar to Bonobos in the percent that wear earmuffs than Europeans.\n\n“The researchers are trying to extrapolate the population history of the Pan ancestor (common ancestor of humans and chimps-bonobos). They do that by estimating the effective population size (individuals of the population that contribute to the next generation) of the Pan ancestor. In order to evaluate the female and male population history (how many females and males reproduce within one population) they calculate the X/A ratio (X chromosome effective population size divided by the autosomal effective population size).\nThe figure shows that the Pan ancestors' X/A ratio is similar to the bonobo and the African one, which practically means that two females reproduce for each male. The European ratio being lower than the rest can be explained by demographic effects of dispersion (migration out of Africa). Those are just evaluations of the population trends and social structures (e.g. female bonobos are observed to move to other groups after maturation, while male bonobos tend to stay to their original group which is reflected in the 2:1 ratio).”\n\nTHEREFORE, ALL HUMANS, REGARDLESS OF RACE OR GENDER, ARE THE SAME GENETIC DISTANCE FROM BONOBOS, AND CHIMPANZEES.\n\nCaucasians (which were defined as Middle Easterners, North African and North Indians) Mongoloids (East Asians) Negroids (Sub Saharan Africans) each maintain a genetic distance of 1.60 from Chimpanzees. That is to say, no specific group of humanity is more akin to chimpanzees.\n\n\nThe chart displayed above was a sample of 1 European and 1 African. There is more genetic variation in Africa than the rest of the world combined. Every human being shares 99.9% of their genome with eachother.\n\n‘Race’ cannot be biologically defined due to genetic variation among human individuals and populations. (A) The old concept of the “five races:” African, Asian, European, Native American, and Oceanian. According to this view, variation between the races is large, and thus, the each race is a separate category. Additionally, individual races are thought to have a relatively uniform genetic identity. (B) Actual genetic variation in humans. Human populations do roughly cluster into geographical regions. However, variation between different regions is small, thus blurring the lines between populations. Furthermore, variation within a single region is large, and there is no uniform identity.\n\nspecies;\nnoun\n1.\nBIOLOGY\na group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding. The species is the principal natural taxonomic unit, ranking below a genus and denoted by a Latin binomial, e.g. Homo sapiens.",
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