RE: The Negroid, And the truth of races
Other 15-point claims
Herrnstein 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).
To 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.
But 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.
And 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:
"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)
It 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.
The 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)
K.R. Vincent, "Black/white IQ differences: Does age make a difference?" Journal of Clinical Psychology 47, 1991, pp. 266-270.
Richard Herrnstein and Charles Murray, The Bell Curve, (New York: Simon & Schuster, 1994), pp. 289-90.
Marilyn Elias, "Experts find fault with 'Bell Curve'" USA Today. (No date given; probably Fall 1995.)
Richard Nisbett, "Race, IQ and Scientism," pp. 50-52 in Steven Fraser, ed., The Bell Curve Wars (New York: HarperCollins, 1995).
Herrnstein and Murray, p. 356.
Ibid., p. 355.
Ibid., pp. 276-77.
Ibid., p. 717.
Nisbett, p. 49. The academic tests used for this statistic are listed in the chart below, which has been compiled from his written account:
Point reduction in black/white IQ gap (1970-1990)*
Test Reduction
National Assessment of Education Progress 4.2 points
Scholastic Aptitude Test 5.0
National High School Studies 4.5
American College Test 4.4
Graduate Record Examination 5.7
*Total reductions have been extrapolated from different-length
studies to represent two decade period. Original lengths: NAEP,
1970-1990; SAT, 1976-1993; NHSS, 1973-1982; ACT, 1980-1991; GRE,
1980-1988.
Impulsivity
Here was a study that linked thrill seeking and impulsivity together and tried to find a correlation with an impulsive behaviour (like drinking).
Racial 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.
Research 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.
Consistent 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).
one potential contributor may be socioeconomic status (SES). Lower SES is related to higher levels of impulsivity.
Even 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.
https://mathcs.clarku.edu/huxley/UnColl/Rdetc/NegPl.html
The 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?
Another study:
“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.”
Several links between sensation seeking and aggression have been found:
https://www.ncbi.nlm.nih.gov/pubmed/20973087
https://www.frontiersin.org/articles/10.3389/fpsyg.2016.01447/full
Whites are also considerably more likely to get stressed than blacks. There have been links with stress and aggression.
https://www.oxfordscholarship.com/view/10.1093/acprof:oso/9780195168761.001.0001/acprof-9780195168761-chapter-12
Child 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.
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.)
Sexual activity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3767847/
https://www.npr.org/templates/story/story.php?storyId=114237523
https://www.latimes.com/local/california/la-me-ln-std-stigma-20180507-htmlstory.html
https://en.wikipedia.org/wiki/Polygamy_in_Christianity#Exceptions_in_Africa
https://jamanetwork.com/journals/jamapediatrics/fullarticle/350980
Is systemic racism to blame?
Los 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.”
The center will target five health disparities, including high rates of STDs among certain minority groups.
Nationwide, STD rates have been climbing for the past five years. More people were diagnosed with syphilis, chlamydia or gonorrhea in 2016 than ever before.
Some 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.
But 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.
Northover 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.
The 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.”
But that’s a tall order given how entrenched many social problems are.
Poverty 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.
“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.
County 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.
“If you keep doing the same thing and expect a different result, then that’s insanity,” Hochman said.
Genes/alleles
MAOA 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.
They 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]
The MAOA-L allele test was never conducted on pure Africans.
https://geneticliteracyproject.org/2014/10/29/genes-linked-to-violent-crime-but-can-they-explain-criminal-behavior/
The 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.
Even 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.
https://www.news.com.au/world/breaking-news/scientists-debunk-maori-warrior-gene-myth/news-story/117e673dd450b9b002d961e39fabc1b6
https://www.mygenefood.com/warrior-gene-5-common-myths/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058761/
Epigenetics and MAOA in the brain
Epigenetics 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].
Various 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].
Elena 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].
In 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].
There 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].
Yet plasticity genes appear to have a cumulative effect.