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Science Daily: Mom’s Exposure to BPA During Pregnancy Can Put Her Baby on Course to Obesity

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Science Daily came out with an article today that exposure to BPA invitro for babies is correlated with obesity at age 7. 94 percent of the women tested had detectable levels of BPA. BPA is also linked with early onset puberty, which I will also speak on later in this article as it has implications for one of my theories.

I briefly touched on BPA in my article What’s the Cause of the Cucking of Europe? where I said:

I advise all of you (women included, there are many deleterious effects of BPA on the mother as well as the baby prenatally), to discontinue use of plastics with BPA in them.

The above-linked study shows that preeclampsia is correlated with elevated levels of BPA in the blood levels in the pregnant mothers, fetal blood, and the placenta. BPA was found to be elevated in mother’s fetal tissue with preeclampsia in comparison to the mothers with lower levels of BPA in their fetal tissue. I will come back to the BPA link with preeclampsia later in the article as it has implications for ethnic groups in America.

The paper, which was just released on the 17th, called Bisphenol A and Adiposity in an Inner-City Birth Cohortcarried out tested BPA in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.** Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors, they discovered that there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period.

The researchers then conclude that BPA exposure invitro “may be an important underlying factor in the obesity epidemic” and that “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.”

If true, this has huge implications for the way we look at the obesity epidemic in this country. Who are the most likely to be obese? “Hispanics” and blacks (Ogden et al, 2014).

Returning to what I brought up earlier about early onset puberty: in my article on the hormone leptin being a cause for earlier menarche in black girls, I noted that since black girls were more likely to be heavier as well as mature faster than white girls, that differences in leptin were the cause of differences in menarche between the two groups.  Elevated levels of serum leptin were correlated with body fat and differences in maturation between the two groups. Differences remained, but lessened, after controlling for differences in fat mass, maturation, age, and physical fitness.

Since BPA is correlated with adiposity in children and black girls have earlier menarche DUE to there being a higher chance of black girls being overweight in comparison to white girls, BPA is yet another piece to the puzzle of this phenomena, along with, of course, evolution. Ingestion of BPA is an environmental factor, however, with these changes in body chemistry in the children invitro due to increased BPA consumption by the pregnant mothers, it leads to one cause that can be prevented from further occurring due to our new knowledge.

The study was carried out on a cohort from NYC. In 2010 in NYC, the city was: 44 percent white, 25.5 percent black, 12.7 percent Asian with the rest being filled out by ‘Hispanics’ (not a racial category) and mixed-race people. Even after they matched for SES and other environmental factors, these differences persisted. However, this study was only carried out on those women who self-identified as either Dominican (basically African) and black. To quote the researchers:

Women were included if they self-identified as either African American or Dominican and had resided in Northern Manhattan or the South Bronx for at least 1 year before pregnancy. Exclusion criteria included mother’s report of: cigarette smoking or use of other tobacco products during pregnancy, illicit drug use, diabetes, hypertension, known HIV, or a first prenatal visit after the 20th week of gestation.

So, we have a full sample of Caribbean Africans and African Americans in this study. What else can we learn about those two populations and their consumption of things with BPA in them?

race differences tap and bottled water

The above Figure (7) is taken from the U.S. Department of Agriculture and the Food Surveys Research Group study on differences in drinking tap and bottled water.in different populations in the country. As you can see in this figure (what is notable is the ages 12-19 and 20 to 60 in the table), whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. However, Mexican American girls, like black girls, are also entering puberty earlier. Since both populations have a substantial percentage of them overweight and obese (factor for serum leptin production which then causes early onset puberty), this again shows a strong correlation between body fat gain and early onset puberty. Moreover, this also shows that both Dominican and black populations consume more bottled water than do white populations, both populations are more likely to be obese or overweight (even after controlling for SES) which causes leptin production earlier causing periods to happen much sooner than in populations who drink less bottled water and use other products with BPA in them. .

Going back to preeclampsia, it is a condition that pregnant women develop that’s characterized by hypertension (high blood pressure) and protein in the urine. It’s known that black women suffer from it the most. More interestingly, over the past ten years, rates of preeclampsia have been increasing in the black female population. As the researchers note in the article, BPA is correlated with preeclampsia. Blacks have a higher rate and chance of being diagnosed with hypertension as well. All of these differing variables coalesce into our current obesity epidemic. With blacks and “Hispanics” being more likely to be overweight/obese drink more bottled water, have a higher risk for hypertension, higher risk for preeclampsia and having earlier menarche, these help explain, in part, racial/ethnic differences in obesity.

These differences can be attributed to consumption of bottled water, i.e., consuming things with made with and packaged in plastic as well as canned foods. From my experience with Dominican and black New Yorkers, they tend to have horrible lifestyles, tend to drink tons of bottled water and also tend to be overweight or obese at a higher rate in comparison to the general population. This leads to biologic factors changing (i.e., earlier menarche in younger girls) in these young girls, leading to devastating effects on their body chemistry.

This study, yet again, proves another underlying factor for obesity in certain populations in the country. And what do you know? It’s the populations that already have the highest rate of obesity in the country. When it becomes definitive that BPA consumption by pregnant mothers does lead to underlying factors in obesity. To quote the researchers: “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.” This will be HUGE for our understanding of underlying causes to obesity! Moreover, if (when) this is fully corroborated, it can then be said that by mothers exposing their children in the womb to excess levels of BPA, there is a chance that they are “giving their own choice to make their children have a higher chance of being obese, as they know the dangers of BPA consumption during pregnancy and all of the negative variables associated with it.”

This is an extremely interesting and important study for our understanding of obesity. Since BPA consumption invitro is correlated with higher fat mass index in girls at age 7, and since those girls who tend to be more overweight and obese than other populations, we can then say that BPA has a hand in obesity in children, which then causes serum leptin to be released, causing way menarche in these populations. An increase in sexual maturation has been linked to the obesity epidemic, which began around 60 years ago. The cause of this is due to the demonization of the fat macro and carbohydrates, all the while it was reversed. This destroyed insulin sensitivity for many Americans, leading to a huge majority of our health problems today.

In conclusion, underlying factors for obesity keep appearing. Due to racial/ethnic differences in bottled water consumption (one of the most common BPA products in households), which the effects of BPA may alter how fat cells are formed in early life, this accounts for, in part, excess adiposity in differing populations. These underlying factors could help show where some of these racial/ethnic differences in obesity come from. Since the two populations in the study (black American and Dominican) both have high levels of adiposity, both drink a lot of bottled water and both have earlier menarche than do whites (who drink LESS bottled water), this shows that some (a lot?) of the variation in obesity between ethnic/racial groupings can be explained by these underlying factors.

** I have one problem with this study. They assessed fat mass index with bioelectrical impedance.The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.

Ethnic Genetic Interests and Group Selection Does Exist: A Reply to JayMan

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JayMan has said that ““Ethnic Genetic Interests” Do Not Exist (Neither Does Group Selection)“. It’s clear from what he says towards the end that he has some sort of bias to attempt to disprove Ethnic Genetic Interests and Group Selection. This will be a definitive refutation of JayMan’s belief of the non-existence of GST and GS. Along with  Dr. Swaggins from the CoonU Blog, both of us today will prove that EGI and GS do in fact exist and that JayMan has an implicit bias in the denial of EGI and GS. I will also address JayMan’s comment to me in that same article that I never responded to save it for this article.

I first wrote an article, Genetic Similarity Theory, in reply to his denial of EGI. It was short, but I got my point across with the Price Equation. JayMan then comments:

Ethnic altruism can’t evolve through genetic similarity because the coefficient of relationship between co-ethnics (who aren’t close family) is pretty small. Even kin selection itself is pretty weak in general. How much time do you spend with your second and third cousins?

In-group favoritism likely evolved through individual selection for reciprocal altruism. Overall similarity simply allowed individuals to recognize likely partners for trading favors (shared language and customs may help). This may have even co-opted systems designed to act towards close kin – misfiring kin altruism, if you will.

Rebutting Jayman’s denial of the ethnic kinship coefficient requires an explanation of the concept of relatedness as a whole. How, for example, can I be 50% identical to my father if I’m 99.8% identical to all living humans? The answer is that I am not 50% identical to my father; rather, I am 50% identical to my father by comparison to the baseline level of relatedness of all living humans. If all living humans are 99.8% genetically identical then I’m 99.9% identical to my father. Jayman’s argument that two random co-ethnics aren’t related fails to factor this into account: a calculation of relation needs a baseline level of relatedness for comparison. So he’s correct in stating that two co-ethnics are not similar to one another- but only by comparison to the baseline level of relatedness of their entire population.

Since the ethnic kinship coefficient has been worked out to the equivalent of half siblings, it may be useful to frame the issue in those terms. If I am 25% identical to my half sibling by comparison to any other co-ethnic, it is because there is a quarter of my genome that I share with my half sibling due to our common descent. Specifically, our mutual descent from our mutual parent gives us a specific combination of genes that nobody else is likely to have. 25% of my genome is 100% identical to his alleles of the same genes and the other 75% is as similar to his as it is to any other co-ethnic, but taken as an average across my entire genome, any given allele is 25% more likely to be shared with him than it is everyone else in our race.

The ethnic kinship coefficient works in an uncannily similar way. Instead of inheriting those 25% identical genes from recent common ancestors, the two co-ethnics inherit the same genes due to the fact that people of their race usually have those genes (think melanin, keratin, microcephalin, EDAR, HERC2, or any other gene for which the frequency of alleles differs overpopulation). In spite of that difference in the origin of ethnic vs familial similarity, the mathematics are shockingly similar: according to Henry Harpending in his review paper Kinship and Population Subdivision, “Many studies agree that Fst [genetic distance between populations] in world samples of human populations is between ten and fifteen percent,” with “a conservative general figure” being 12.5%. What’s more, Fst “is computed for each allele at each locus, then averaged over all loci.” In other words, 1/8th of human genetic diversity is at the between-group level.

To put things into perspective, a 1/8th reduction in diversity within a family occurs when two half siblings (25% identical) have a child. There is a 1/16th chance that the common parent will pass a given allele to both children and that both children will pass that allele to their child, and a 1/16th chance for the same to occur for the other allele of the same gene; when computed allele for allele, “diversity” (odds of heterozygosity) goes down by 1/8th among a population that is 25% identical by descent.

One such calculation finds, for example, that a Frenchman is 24% identical to another Frenchman if your baseline for comparison is the genetic similarity between the French and Japanese.

This is the inevitable implication of the central tenet of HBD: that the various races of the world are genetically different from one another. It is also the inevitable implication of Lewontin’s famous finding that 15% of all human genetic variation is racial; if it were 100% then all co-ethnics would be identical and it were 0% then race wouldn’t exist at all. If it were 15%, though, then that 15% would be composed of genes whose alleles vary in frequency across populations; these are genes you share with co-ethnics much more often than you share with anyone else. If you’re more likely to share a lot of genes with co-ethnics than you are with anyone else, then you’re more genetically similar to co-ethnics than you are anyone else. When they sequence the genes of people of different races and compute the odds of similarity locus for locus, you’re much more likely to share some genes (ABCC11, MC1R, etc) with co-ethnics than you are others, but taken as an average across both copies of the entire genome, it’s about 25%. Apply those odds to the 20,000 or so genes in the human genome and the result will be consistent with the data that members of a given race are about 25% identical by comparison to members of other races.

We are not the first people to predict that these genetic differences would result in kin selection expressed as altruism towards co-ethnics and discrimination towards others; to quote an article by the late Henry Harpending posted in March 2012, “In the new diverse community the average person can find someone related as f~0.06, corresponding roughly to a great-grandchild at f=1/16. Suddenly there is a fitness payoff to discrimination.” (In this hypothetical population, an individual is 1/8th more related to a co-ethnic than to the average and 1/8th less related to some of a different race than to the average.) In an ethnically homogeneous population, discrimination of this kind will not occur because the fitness payoff of benefiting one co-ethnic or the other is the same, but in a heterogeneous population, you suddenly have people in whom you have comparatively more or less genetic interest. In December 2012, Harpending and Salter published “JP Rushton’s Theory of Ethnic Nepotism,” a paper predicting that the Fst data would support Rushton’s theory of ethnic genetic interest, by providing evidence for kin selection. Towards the end of this article, I will provide evidence for human altruistic behavior fitting the patterns predicted by kin selection, and I will present a likely animal model for subspecies competition over resources. In the meantime, however, there are more misconceptions to clear up.

JayMan says:

I suppose a key misunderstanding in the matter is the failure to realize that each individual gene contributes to fitness independently. Each gene is “out for itself”, so to speak. It just so happens that in any given organism, genes achieve success by working together (most of the time). As sucheach individual gene’s “aim” is to make more copies of itself. What’s going on in the rest of the genome is tangential to this. ((—>Each gene would be just as happy to mix with any other gene, so long as its own fitness is increased in the process.<—))  (Additions in last sentence for emphasis are mine)

Individual genes don’t always contribute to fitness independent of one another; the venerable Nicholas Wade has pointed out that there is at least one gene which confers different levels of selective disadvantage depending on the other genes they’re mixed up with: an allele that slightly increased risk of heart problems in Europeans causes big problems whenever it introgresses into Africans. Naturally, the population which has had this allele for longer has more genes elsewhere in the genome compensating for its negative effects, meaning that said allele will cause fitness problems after it introgresses into another population. Introgression is just a fancy word for race mixing, though, and there are other problems with it, as follows:

In a study of 100,000 mixed-race adolescent school children, those who identified themselves as such had higher health and behavior instances than those of one race. The effect was still observed even when SES and other factors were controlled for. A problem with an obvious genetic component.

Yet another study done on white-Asian mixes notes that they have a two times higher rate to be diagnosed with psychological problems such as anxiety, depression and substance abuse.

It was found, in agreement that black-white mixes engaged in more risky behavior than did monoracial children. They also observe that mixed-race adolescents are stark outliers in comparison to whites and blacks, which still holds true despite being raised in similar environments to monoracial children.

Fitness doesn’t look increased in that process, seeing how mulatto children show more health problems and negative behavior than monoracial children. And given the data relating to the allele mentioned above, we can’t rule out the possibility that health problems in biracial children arise because their parents’ genes don’t necessarily work together.

There is no impact on one’s fitness from the race of one’s mate (or an offspring’s mate) so long as close relatives are off the table as mates (aside from the fitness impact of the particular genes such mates were bringing in the environment in question). The fitness impact to a White man’s genes if his daughter marries a Black man is the same as if she married an unrelated White man (again, fitness from gene function notwithstanding).

Do you really believe that? As shown above, mixed-race children show more health and behavior problems than do monoracial children. Africans were not selected for resistance to the negative effects of certain European genes as Europeans were, and we have no reason to believe that any race is selected to compensate for the negative effects of genes they don’t even have.

Just the same, the inclusive fitness impact to a White American is the same whether he focuses his altruistic act on an unrelated White American or on a Namibian; it is zero in both cases. If you adopt children rather than have your own, the fitness hit to you is the same whether your adopted children are White, Black, Chinese, or Venezuelan.

Again, this assumes that there are no genetic differences between populations, but there are, so your fitness is probably higher if you adopt a co-ethnic than if you adopt someone else.

Hence, there is no human ethnic group that exhibits ethnic nepotism. This includes Ashkenazi Jews. But these have nothing to do with ethnic nepotism, didn’t arise via kin selection, and don’t depend on genetic relatedness per se. This includes Ashkenazi Jews.

Ashkenazi Jews evolved their nepotism through thousands of years of getting driven out of countries. Along with being barred from certain jobs, this led to them being only able to do banking jobs and those jobs that took more intellect, which they then evolved their higher IQ as well as more group favoritism to help them in societies where they are the minority. This is clearly evident today with Jewish overrepresentation at elite universities; their average IQ of 110 suggests that they shouldn’t be that much of the student body since they’re six times as likely to be geniuses but many more times likely to make it into the top institutions. Odds are pretty good that that’s ethnic nepotism in action. We’re talking about a group of people 38% likely to consider themselves religious but 70% likely to believe the old mythos that the omnipotent, omniscient creator of everything that ever existed prefers them to literally everyone else, and judge whether someone is worthy of this inconceivably lofty status purely on the basis of their genetics; before they had handy-dandy PCR machines and enzymes, Jews determined someone to be Jewish by matrilineal descent, not cultural custom. If the Ashkenazim lacked any ingroup preferences of any kind during their time in Europe, they would’ve literally copulated themselves to death by marrying Gentiles until their population was totally absorbed by ours. What would you call it then, JayMan, if not EGI? They’re one of the best examples FOR the existence of EGI. See, the thing is, if someone is an Ashkenazi Jew, more often than not, they will be more related to each other than some other random person from another population.

This particular fact – that co-ethnics share genes – is why they have a genetic interest in one another.

The Ethnic Kinship Coefficient has been corroborated literally every time anybody calculated Fst values between different human races, and by JayMan’s understanding of kin selection it disproves his assertion that ethnic genetic interests do not exist:

This [relatedness] is the probability that a given relative of an individual possesses a copy of an allele the individual possesses.

Co-ethnics are about 25% more likely to share the statistically average allele than people of different races are, so the Hamiltonian drive to confer benefit on co-ethnics is comparable to the drive to confer benefit on secondary relations (half siblings, grandchildren, etc). In other words, it doesn’t matter that the frequency of altruistic alleles is unaffected by the presence of outsiders, because people have a genetic imperative to assist the genes they share with their co-ethnics either way (and are therefore selected for altruism/ethnic nepotism either way); since they are related to their co-ethnics regardless of context, they are selected for the desire to confer benefit on co-ethnics regardless of context, and they only have a genetic interest in derogating an outgroup if doing so will increase the fitness of the ingroup. This is why Harpending and Salter observe, in the paper linked above, that racial solidarity “strengthens in response to attacks perceived to be aimed at group identity, especially invasion of the homeland and physical harm done to co-ethnics.” Observe Donald Trump or Marine Le Pen excoriating the bureaucrats they deem responsible for an alleged invasion, or Black Lives Matter being more enraged about a Hispanic killing a black than by thousands of blacks killing thousands of other blacks. A supposed shift in altruistic allele frequencies was never the point, and to argue against it is to battle with strawmen.

If altruism is the result of kin selection, then an organism will confer benefit on the criterion of relatedness. If a European man saves a daycare with 8 Asian babies in it from some freak accident, then he saves as much of his own genes as were shared by those babies. If he saves a daycare with 8 European babies in it, he just saved a collection of his own copies of HERC2 or ABCC11 or EDAR or some other such gene which he previously failed to save as well. If he saves 8 of his co-ethnic first cousins, the proportion again goes up, this time by 12.5%. By the same mathematical model we use to explain kin selection (Hamilton’s Rule), we predict and observe that altruism will be expressed to various degrees depending on the degree of relatedness.

The adaptation to this would have nothing to do with magical altruism genes which change in frequency when Japanese people arrive in France. Rather, the selection pressures predicted by the kin selection model would select for organisms that exhibited compassion and cooperation in proportion to relatedness.

The fact that co-ethnics share so many genes means that they do have a genetic interest in one another, if kin selection is real. I personally believe that kin selection is a clearer and more likely explanation for altruism than group selection in most cases, but due to the difficulty of determining causality in processes that occurred thousands if not millions of years ago (namely the original evolution of altruistic behavior), I doubt that the scientific community can put this one to bed yet. For the purposes of this issue, however, JayMan has already professed his belief that group selection has never occurred, meaning that one of a few different things must be true.

  1. Humans are not altruistic at all. Untrue.
  2. Humans are altruistic, but not due to kin selection or group selection. Unlikely; we can talk about mutual back-scratching all we want but the fact that people take bullets and jump on grenades for one another means that mutual benefit cannot be our only reason to confer benefit upon others.
  3. Humans are altruistic due to kin selection. This explanation is consistent with genetics and evolutionary theory; evolution holds that survival is a matter of passing on genes and genetics show that related organisms have many of the same genes. It also has pretty good predictive power (it predicts familial love, racism, and other real phenomena). For these reasons, I’m going to be arguing from the assumption that kin selection is a primary reason for human altruism, and that it, therefore, must exist in humans.

Due to the genetic similarity between co-ethnics, there is a genetic interest between them. Each has a Darwinian interest in the other comparable to roughly 25% of their own survival. Operating from the assumption that kin selection is the reason for human altruism, one would predict one of the following possibilities:

  1.  Humans will prefer to confer benefit to their co-ethnics over others due to the fitness advantage gained by doing so,
  2. That humans cannot perceive genetic similarity and have therefore been selected to benefit one another regardless of genetic similarity in hopes that they hit the mark by accident,
  3. Humans do prefer those who are genetically similar but are incapable of perceiving the genetic differences between the various human subspecies, or
  4. Humans understand the genetic differences between themselves and others but for whatever reason will not take the 25% fitness advantage. I’m going to go ahead and throw this one out.

We know that humans prefer others on the basis of genetic similarity, and we know that nearly all human cultures have considered those of different ethnicities to be “the other,” or at least different in some significant way. We know that people can determine someone’s biological race based on their appearance, in any case, and in his 1996 book Race in the Making: Cognition, culture, and the child’s construction of human kinds, Lawrence Hirschfeld found that even children could do so. All of which means that humans can get a rough idea of genomic similarity (or difference) using phenotype and family history as a proxy, and that race is among the types of genetic difference that humans are capable of perceiving. If humans prefer one another based on the criterion of genetic similarity (they do), and race is a genetic difference that humans can perceive (it is), then we expect humans to generally prefer those of their own race (they do).

Even in studies of bereavement, Littlefield and Rushton (1986) put forth ten hypotheses (I will only bring the ones up that prove the case for EGI) to make the case for Genetic Similarity Theory:

  1.  A mother will grieve more than the father: this is due to the mother having  finite number of ova, have a more limited reproductive potential than do men and also bear the burden of bearing children, this shows that each offspring of a mother is more important to the overall success to her genes than the are to the father’s.
  2. Male children will be grieved for more intensely than female children. This is due to a male having a higher chance to have more children and spread his genes to more progeny.
  3. Similar children will be grieved for more intensely than dissimilar children. GST explains the phenomenon of assortative mating, the phenomenon that spouses will be genetically similar on those traits more influenced by genetics. One consequence of assortative mating is that one parent may be more similar to the child than the other. This can be illustrated as follows: Rushton and Littlefield: “If a father gives his child 50% of his genes, 10% of which are shared with the mother, and the mother gives the child 50% of her genes, 20% of which are shared with the father, the child would be 60% similar to the mother and 70% similar to the father (Rushton et al., 1984)”. So we can see that depending on the amount of genes a child gets from his parent will infer whether or not they are genetically similar to which parent, and in the case of a possible surprise death, the parent who believes the child looks (shares more alleles in common with) like their selves, will grieve longer and more intensely due to having a greater fitness hit due to the increased GST.

This study shows good evidence that the more genetically similar the child is to the grieving parent, the more strong and intense the grieving process will be. How mothers and fathers will risk their lives for their children, their genetic endowment, shows another truth to this phenomenon: altruism. Altruism for those who are genetically similar to yourself. We can then take this and show that since co-ethnics are closer to each other than they are to distant populations, and that since they are more genetically similar to themselves, the same kind of derogation and suspicion that parents give strangers who come around their children, co-ethnics will give to non-co-ethnics when they appear in their homeland. Robert Putnam’s research corroborates this.

Altruism/nepotism does increase when out-groups come to the land. When this occurs, the native population of the country will, in theory, become more altruistic to co-ethnics since their genetic interests are at stake. This is currently occurring in Eastern and Southern Europe in countries like Hungary, Poland, Spain, and Italy.

The model has pretty good predictive power since it predicts racism and other phenomena, which I’ll dive into now. Applying the kin selection model to humanity we expect that altruism will not only be doled out proportionally with respect to genetic similarity, but also to the number of babies the recipient is likely to have. I wouldn’t do as much for my DNA by saving the residents of a retirement home as I would by saving a daycare. And saving women is smarter than saving men. Hence, when the Titanic sinks, the rallying cry of the day is literally “save the women and children!” (Because the people who didn’t do that throughout our biological history had less of an impact on our gene pool than the ones who did.)

So you’re going to see innumerable charities for the benefit of children, and comparatively, nobody trying to solve the conundrum of how terrible life is in nursing homes for the elderly. On the Forbes list of top US charities, numbers 1-4 all frequently work with children (as do many others) and numbers 5, 6, 12, and 14 are specifically for children. None of them are specifically for the elderly; making sure that Grandpa isn’t miserable and alone registers nowhere in the top 50 items of our society’s to-do list.

And you’re going to see things like this, in spite of the fact that men are equally likely if not a hair more likely to get lung cancer and it’s a big killer in both sexes because people care more about “women” than they do about “people.” And I’m not joking or cherry-picking: Lung Force’s blog is seemingly more about women’s feelings than about lung cancer, no doubt because these people are aware that breast cancer research receives way more funding than prostate cancer research does in spite of similar death rates . In other words, it’s a well-known fact among people whose jobs are to stir up altruism that people will give more resources for the well-being of women than for the well-being of men.

All of which is just another case of altruism that “just so happens” to confer group and/or kin benefit, and does so proportionally to the expected increase in fitness, precisely as kin selection would predict. I would expect people to donate more to co-ethnics as well, were it not for the facts that:

a) It’s fashionable in our society to virtue signal niceness to swarthier folks, and

b-z) Haitian children literally eat dirt for breakfast.

In any case, you can look at where rich nonwhites send their donation dollars, be it the fitness benefit gained by JayZ when he donates to clean water causes in Africaor by George Lopez in his “contributions to the Latino community“. This isn’t a cherry-picked trend of statistically irrelevant anecdotes: Blacks donate to other Blacks, “Identity-based giving is gaining momentum in the Latino, Asian American, Arab American, and Native American communities,” and “Latino’s motivation to give is embedded in a sense of responsibility and desire to give back to their community.” Much of the work of such people may end up benefiting Whites who happen to be there when a catastrophe hits a bunch of the donor’s co-ethnics (observe a Black donating to Hurricane Katrina; New Orleans is majority black, but not devoid of Whites), or occasionally they’ll donate to other nonwhites. But I’m not holding my breath for the day they raise awareness for the White squatter camps in South Africa.

Basically, any time that a person does a nice thing for another person, it will be proportional to any combination of three factors: genetic similarity, assumed number of offspring, and/or how bad the recipient needs help. All three of these are predicted by kin selection since all three are factors which predict the fitness gained by engaging in an altruistic act.

Importantly, virtually every culture on Earth preferred co-ethnics to others prior to the Communist subversion of the West, at which point accusations of racism became something of a social death sentence. (You don’t believe me on the Communist subversion thing- think it’s a conspiracy? Google up where all of this “social construct” ideology we keep encountering ultimately came from, and look up who’s promoting it today.) One could claim that whether a culture is “racist” or not depends on “culture” rather than biology, and point to the modern West as an example of an “anti-racist” culture, but in that case, it’s one hell of a coincidence that every race on Earth generally preferred themselves to everyone else, and did so for 10,000 years or more if you count prehistory. Considerably more likely is that populations with no ingroup preference are subsumed by other populations who gain a fitness advantage by doing so (they mounted no defense because they didn’t understand the need to do so) and that the majority of modern humans are therefore descended mostly from passionate racists.

Co-ethnics have a real genetic interest in one another due to large amounts of shared DNA, meaning that ethnic genetic interest is real. Humans do act on genetic interests in general, as the family studies show, and they are capable of perceiving racial genetic differences, as the ethnicity studies show; it is, therefore, likely that they will act on these ethnic genetic interests as they do with other genetic interests, because racism is caused by the innate preference for genetically similar people. In other words, racism is a biological phenomenon instead of a cultural one.

That, or nearly every culture ever in the history of forever was racist by pure coincidence.

To put subspecies competition into perspective, I will point out that wolves and coyotes have a Fst value between 0.056 and 0.121 and can interbreed. We can call subspecies and other taxonomic classification a social construct if we like; technically we’d be correct in the case of canids, to whom the words “species” and “subspecies” are doled out in a pretty arbitrary fashion. We can say that the admixture is proof that the wolf and coyote DNA doesn’t care about which other genes it’s combined with, if we like. But everything we say about it does absolutely nothing to change the fact that the biological fitness of coyotes massively drops when they share territory with wolves.

Understatement of the week: the implications of having to compete for the same resources is probably why canids fight for territory. Wolf packs, being direct family, would no doubt have a high Fst with other wolf packs, no different from how I’m more similar to my grandpa than I am my housemates. They fight for territory on a familial level because of genetic interest, and they have been observed fighting for territory on the level of subspecies as well, with a clear genetic interest in doing so. The only difference between them and us in this respect is that our method of acquiring resources relies on commerce rather than hunting, and so we weren’t selected for the propensity to wander around a given territory fighting off other families who intrude. That’s not good for business; in fact, I’d be willing to bet that warfare usually occurs in humans when the profit incentive for conquest is greater than the profit incentive for trade. Humans who don’t engage in a lot of commerce and belong to inbred populations, though, have fewer incentives towards peace and higher Fst values relative to others- and they aren’t above killing the guys from the next tribe over. What a surprise that these village’s conflicts had to do with territory and breeding, both of which have to do with fitness. In any case, humans from populations selected for agriculture and commerce engaging in this sort of behavior is the exception that proves the rule, because the only reason anybody knows about the interfamilial warfare of the Hatfields and McCoys is that it falls under the “man bites dog” rule.

I have this radical view that biological rules still apply to humans, and that we are therefore self-replicating bags of meat smart enough to understand that we are self-replicating bags of meat. I see little difference between wolves reclaiming their old hunting grounds and the Reconquista movement. Coyotes had taken over when the wolves kept getting killed by men; Spaniards took over when a storm of viruses killed off most of the Natives. Even after the Spanish admixture, the Fst values between Whites and the now-mestizos likely falls within the range of coyote-wolf Fst values. Wolves feed their kind with elk and we feed ours ultimately with money; the distribution of elk meat to wolves isn’t good for coyotes and I’m willing to bet that the distribution of money and jobs to other nations and their peoples explains much of our abysmal birth rates in the West (with birth control technologies being another primary factor). We had lots of kids back when there were blue collar jobs you could get fresh out of high school which instantaneously elevated you to the middle class. We could afford to have them, no different from the fact that European nobles had more kids on average than us commoners. If current economic, cultural, and political trends continue, though, then ethnic Europeans might go out roughly 50x faster than the Neanderthals did.

Biological organisms show preference of those who are similar at the level of self (me), family (the Kennedys), tribe or nation (Papuan tribes or Mexico), race or subspecies (Native Americans), and species (I eat pork and kill spiders more often than I eat aboriginal Australians and kill Sentinelese people). All are the same phenomenon (attempts to increase the odds of self-replication at the genetic level), all are predicted with Fst values and Hamilton’s Rule, all are observed in animals to whom “culture” doesn’t apply, and all are observed in mankind.

Now, the question is this: how would GST be detected? Numerous ways. Location, for one. Since up until around 50 years ago, most countries were monoracial, those in your general proximity will, more often than not, be more genetically similar to you than a group that’s 50 miles away. Culture, which is an expression of genetics, is yet another way that GST can be detected. Since culture is an expression of genetics, when that culture is expressed, this shows other genetically similar co-ethnics that this individual shares more genes in common than those who don’t share their culture. There is also matching by phenotype, which goes along with the location aspect. But, as I stated in my article Genetic Similarity Theory as a Cause for Ethnocentrism:

It’s clear that we are more altruistic to people who look more phenotypically similar to ourselves, to pass on and benefit copies of our genes. This evolved in spite of the negative impact on behalf of the altruist. The altruist is helping copies of his shared genes survive so that they may be copied into the next generation of progeny. The tendency to favor co-ethnics is the tendency to attempt to help pass on shared genes, as if the phenotype is similar, more often than not, the genotype is as well. This is the basis for ethnocentrism.

There is also what is called the “Grandmother’s hypothesis” in which the researchers theorize that women live past menopause to help take care of their grandchildren. In doing so, they can then make sure their grandchildren are well-fed and nourished. The researchers state that by using Hamilton’s relation coefficients (what we have been using in this article), that a grandmother should share 25 percent of genes with her grandchildren. Ted Sallis says:

Therefore (and this is the important point), a paternal grandmother, all else being equal, is genetically less related to a grandson than to a granddaughter, and less related to a grandson than is a maternal grandmother.  Conversely, a paternal grandmother likely is more genetically related to a granddaughter than is a maternal grandmother, given the certainty that the granddaughter possesses an X chromosome from the paternal grandmother.

The researchers hypothesized that the grandmother’s investment in grandchildren will be directly mirrored by how genetically similar they are to each other. The authors conclude that women live past menopause to help care for their children’s offspring. Since they share 25 percent of their genes with their grandchildren, they too, have a genetic investment in making sure they get adequate nutrition and are well cared for. They found that in 7 previously studied populations that “separating grandchild survivorship rates by sex reveals that X-chromosome relatedness correlates with grandchild survival in the presences of MGMs and PGMs. In all seven populations, boys survive better in the presence of their MGM than PGM. In all bar one population, the PGM has a more beneficial effect on girls than on boys. Our X-linked grandmother hypothesis demonstrates how the effects of grandmothers could be sex-specific because of the unusual inheritance pattern of the X-chromosome.”

This is what this whole debate is about: ability to detect genetic similarity in co-ethnics. Matching by phenotype, culture, and general proximity will, with good chance, bring you together with someone who shares more alleles in common with you and someone who you would feel more altruistic towards since you have a genetic interest in ensuring that some of your genes survive to the next generation.

Mixed-race relationships don’t discredit the existence of EGI/GST, in fact, it helps to strengthen it. Americans of mixed ancestry made up for ethnic dissimilarity by matching up on the more heritable traits, whereas the correlation is lower for those traits that are more influenced by the environment. Since the correlation is higher for heritable traits, i.e., BMI, personality, alcoholism, aggressiveness, criminality, psychiatric disorders and so on. Since the correlations are higher than in the environmentally mediated traits and since mixed-race couples match on more heritable traits than on the traits more influenced by the environment, this shows us that even though they are marrying outside of their race/ethnicity, they still match up on the more heritable traits and not the traits more influenced by the environment. 

JayMan brings up the concept of reciprocal altruism as if it negates the effect of racial/ethnic altruism as a whole. It does not. Reciprocal altruism and  Genetic Similarity Theory go hand-in-hand as genetic similarity eliminates the need for the reciprocation to occur again. Since two related individuals share more genes in common with each other than two unrelated individuals, this then caused reciprocation and GST to evolve hand-in-hand with each other. To quote Rushton:

Thiessen and Gregg (1980) make the same point. Thiessen and Gregg state that “cooperation among `nonrelatives’ (`reciprocal altruism’) may be based in large part on genetic and phenotypic similarity” (p. 133).

Another reason that GST and reciprocal altruism go hand in hand is that genetic similarity at certain important loci can predict the efficacy of a reciprocal altruistic relationship; Fowler & Christakis find that close friends are as similar as 4th cousins, and Guo et al find the same for spouses. Selecting for phenotypic compatibility means selecting for genetic similarity at the loci which determine the relevant phenotypes (height, IQ, personality and so on). For example, different races of the world differ in Big Five personality traits, and the reason for these differences is likely genetic. If a statistically normal, introverted East Asian prefers to associate with fellow introverts, what are his odds of becoming best friends with a comparatively gregarious Black man? A gregarious Asian or an introverted Black may become fast friends with those of other races, but most of their kinsmen are more stereotypical.

Ultimately, however, what it comes down to is this: if a gene can better ensure its own survival by bringing about the reproduction of family members with whom it shares copies with, then it can also do so by bringing about the reproduction of any organism that it shares genes with. Meaning altruistic self-sacrifice. But, if there is a fitness gain for the altruist, then how is it altruism? Simple. The altruist is just protecting genetic interests. The altruist is just being driven by his genes to save copies of itself. This is basically what we humans are: organisms that only attempt to bring about those with similar genetics to ourselves.

Racial differences in Blood Donation

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Racial differences in blood donations pose a big problem for minorities. This has to do with altruism, which as I have covered extensively here, has a genetic basis. This pathological altruism has whites give and donate more than other races. This is due to evolving in colder climates with harsher environments, which high intellect evolved so our ancestors could survive. Why do minorities, blacks specifically, donate blood less?

Shaz and Hillyer (2010) observed that minorities were underrepresented as donors in the U.S., and that the cause was a higher deferral rate. Deferral reasons include: “low hemoglobin, travel, abnormal blood pressure, pulse or temperature, inability to find vein, tattoo/piercing, infection or taking antibiotics, and not being in good health.”  They state that blood donation rate for blacks was 25 to 50 percent of that of white individuals.

Blacks have lower levels of hemoglobin than whitesThe Red Cross defers people with low levels of hemoglobin. I don’t really know about blacks traveling too much. Abnormal blood pressure could be low or high blood pressure. Your blood pressure is determined by the amount of blood your heart pumps and the amount of resistance in your arteries.The more blood your heart pumps while arteries are clogged, the higher your blood pressure will be. The more fat and cholesterol that build up on the inner walls of the arteries, which I covered the other day, is called atherosclerosis. Called “hypertension” by the medical community, blacks also have a higher rate of this disease as wellBlacks have more genes expressed for coronary artery calcium, which is a strong indicator of atherosclerosis burden. Cardiovascular disease, more specifically coronary heart disease (CHD) is the leading cause of death for all Americans of all ages and ethnic groups (smoking is a leading cause of this). Blacks suffer the highest percentage of deaths due to CHD. And finally, inability to find a vein is due in large part to 75.6 percent of the black community being obese in America (69.2 percent for men and 82 percent for women).

Another reason for deferral is that all though Sickle Cell Disease isn’t strictly a racial disease, blacks do have the highest rate of it. Those with Sickle Cell Trait (SCT) can donate blood, though those with Sickle Cell Disease cannot.

Infections and antibiotics as well as not being in good health is yet another reason why blacks get deferred. This is due in part to “down-low bruthas” who are more likely to have diseases, and therefore cannot donate blood or plasma. Since homosexuals have some of the highest rates of disease in the country, it’s no surprise that blacks would be leading the pack in that subgroup of the country as well. This is a huge reason why blacks get deferred so much. However, in December of last year, the FDA lifted its lifetime ban of gays donating blood. I shutter to think what the deferral rates of blacks will look like in a few years due to this. That is also why “not being in good health” along with “infection or antibiotics” are such big reasons for deferrals. Blacks have all of the things they defer for, yet of course, allegations of prejudice and racism come about and the government has to step in to change things again, endangering the citizens of the country.

blood

To quote from this AmRen article:

It has long been known that blood transfusions and organ transplants work best between people of the same race. Until the Second World War, stocks of blood were routinely segregated by race for this reason. Classification by race was ended when it was discovered to be “racist,” but blood banks are reinstituting segregation.

The distribution of the common blood types is different from race to race, and some rare types are unique to certain races. Only blacks have U negative blood; only whites have Vel negative or Lan negative blood. Dr. W. Laurence Marsh of the New York Blood Center justifies racial classification: “It makes no sense to screen 100,000 whites for U negative when no U negative white person has ever been found.”

So there is a problem with interracial blood transfusion, and they work better with co-ethnics than non-co-ethnics.

The Central Blood Bank states this about ethnicity and blood donation:

Though compatibility is not based on race, genetically similar blood is best for patients who need repeated or large volumes of blood transfusions, or those who have produced red blood cell antibodies for various diseases and conditions like sickle cell, heart disease and kidney disease.

It says that “compatibility isn’t based on race” then says immediately after “genetically similar blood is best for patients who need repeated or large volumes of blood transfusions. . .” The fact that there are differences in blood-type rate by ethnicity, and that there is a shortage of those blood types for blacks and “Hispanics” in America.

There are varying frequencies in white blood types are found in ethnicities throughout the country, and these varying frequencies in blood type are another reason why interethnic blood transfusion cannot happen; because the differing ethnic groups vary in the different blood types, there will be a low chance of having a certain blood type if it’s rare.

Another reason why blacks donate blood less is due to fear of needles and low iron. Low iron is due to vitamin and mineral deficinecies in diet. Combined with all of the aformentioned variables, this is why blacks get deferred so much. They just don’t donate as much either.

The disparity in differences in blood donation also come down to differences in giving between the races. Whites were seen to be more altruistic than were minorities in the study. This same altruistic behavior leads to more blood donations, but it also leads to the cucking of Europe due to the increase in pathological altruism.

Racial differences in blood donation are due to a whole host of factors, mainly being SCD and other diseases as a barrier for donation, as well as differing blood type frequencies between ethnic/racial groups. Since blacks have higher frequencies of SCD, SCT, and SCA this is another cause for their deferral rate. Being highly sexually active leads to higher disease acquisition, which is another reason less blacks donate blood.  Moreover, blacks’ want to donate will not increase either; racial differences in blood donation and problems will persist to the forseeable future.

Gene Expression By Race

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Since all humans are less than 1 percent different, many people take this to mean that “Race is a social construct“. The stranglehold that race-denying individuals have had on our society for the past fifty years has had huge implications for our society. This egalitarian notion that “we are all the same” together with affirmative action has already begun its devastating effects on our society with this “Blank Slate“, “ghost in the machine” way of thinking.

However, when they engage in this fallacious reasoning, they fail to realize that we are 96 percent genetically similar to chimpanzees. They also don’t know that cats have 90 percent homologous genes with humans; 82% with dogs; 80% with cows; 79% with chimpanzees; 69% with rats and 67% with mice90% of the mouse genome could be lined up with a region on the human genome99% of mouse genes turn out to have analogues in humans. We  share 97.5 percent of our DNA with mice (which is why lab tests get carried out on them). All of this data makes it clear: what causes phenotypic differences between species that are so genetically similar is not how much genetic distance (Fst) is between them, but how those genes that differ are expressed between these populations. Knowing this, it doesn’t seem so crazy now that with less than a 1 percent difference in the genome on average between the races that there are ways to see that race exists genetically. Moreover, the fact that geneticists estimate that there is a difference of 3 million base pairs between two humans on average, shows that there are enough genetic differences between human populations to produce phenotypic differences to be able to differentiate human populations and that since genotype is the cause for the phenotype, due to the physical diversity between human populations that it doesn’t matter how “small” these differences are, but, as mentioned previously, how those differing genes are expressed is the proof that race exists.

Cheung and Speilman collected the gene sequence of a particular white blood cell in 82 Asians and 60 Europeans. They found that the amount of genetic differences was minute, though the two races had differing amounts of gene expression. 25 percent of the overall genes tested showed differing expression between the Asians and Europeans in the sample. It was noticed on one gene that Europeans expressed it at 22 times the strength that Asians did! Since Asians and Europeans split off around 40 kya, I wonder what a study done on Europeans and Africans would show in regards to gene expression strength along with overall differing genetic expression between those two races.

Hicks et al (2013) compared gene expression levels in 4 populations (whites, blacks, Asians and ‘Hispanics’). The gene expression data consisted of 126 whites, 51 ‘Hispanics’, 13 blacks and 8 Asians. They discovered that there were 300 significantly identified genes that showed differing expression in the four populations tested. Some of the genes were: PHF6 (“Mutations affecting the coding region of this gene or the splicing of the transcript have been associated with Borjeson-Forssman-Lehmann syndrome (BFLS), a disorder characterized by mental retardation, epilepsy, hypogonadism, hypometabolism, obesity, swelling of subcutaneous tissue of the face, narrow palpebral fissures, and large ears.”, BRD3 (observed to be implicit in some forms of leukemia, as well as performing cell overlapping functions), CRLF2 (“. . . which control processes such as cell proliferation and development of the hematopoietic system. Rearrangement of this gene with immunoglobulin heavy chain gene (IGH) on chromosome 14, or with P2Y purinoceptor 8 gene (P2RY8) on the same X or Y chromosomes is associated with B-progenitor acute lymphoblastic leukemia (ALL) and Down syndrome ALL.”) and finally RNF135 (known to be involved in protein-protein and protein-DNA interactions). All though this study had an extremely small sample size for Asians and blacks, with further study in the future, we will see bigger sample sizes to better test these predictions.

Analysis of 639 tumor samples (270 black, 369 white), showed that 95 genes were overexpressed involving prostate cancer from blacks relative to whites and 132 were overexpressed in whites relative to Asians. This seems like testosterone is correlated with this as well. Since blacks are twice as likely to get prostate cancer than white men, this shows another reason why there is a disparity in disease acquisition between races: genetic differences, not any allegations of racism people attempt to use.

Still, there are differences in gene expression that account for more disease rate differences between blacks and whites. Huang et al (2011) observed gene expression differences between blacks and whites that lead to atherosclerosis. They discovered 409 differently expressed genes. Genes expressed lower in black Americans also tended to express lower in blacks with lower CAC. Ontological analysis also verified that of the 409 race-associated genes, a significant amount of them “revealed significant enrichment in mobilization of calcium and immune/inflammatory response”.

With differences in testosterone, estradiol and other hormones between the races, as well as looking at disease rates between human populations and studying what genes correlate with what disease, we can better understand human evolution as well as develop new and specific drugs for individuals based on their genotype.

The gene ACTN3 has been linked to athletic performance, specifically sprinting. Those descended from West African populations have it, i.e., Jamaicans and other Caribbean Islanders along with West Africa. 70 percent of those individuals have this gene variant, so, due to this, the all-time record holders in sprinting are all descended from West African populations. This holds true for Europeans as well. This is seen in World’s Strongest Man (WSM) competition wins by country, seeing as the countries with the most wins have majority white populations. A white man has also won the WSM every year since its inception, which is yet another example of gene expression in action.  Whites and Asians have more slow twitch fibers (along with Kenyans) and West African descended blacks have more fast twitch fibers, accounting for these genetic differences which then manifest themselves in our athletic competitions.

Race does exist, and average phenotypic variation is the proof that there is a biological reality to race. The races differ in disease acquisition, as well as muscle fiber typing, which then accounts for disparities in professional championships won along with racial differences in the racial mix of certain sports. As we begin to fully understand the human genome, we will then begin to understand how and why the races differ genetically. The fact that the races differ, on average, on genetic expression shows that there is a reality to what we call “race”. Yes, race is a “social construct”, but it is a social construct of a biological reality. To put it simply, everything is a social construct, and if race doesn’t exist because it’s a social construct then nothing exists, since everything is socially constructed in our minds. But, we know this is not the case. There is a reality, and we use science to test that reality and confirm it with the scientific method.

Can You “Hear” Race?

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I’ve been wondering about this for a while now. Whenever you hear a black speak, nine times out of ten, you can tell whether or not it’s a black who is speaking. The differences come down to testosterone and morphological differences in vocal cords.

This study compared vocal tracts in 140 white, black and Asian speakers who were divided amongst the three races. The researchers controlled for age, gender, height and weight. They measured six dimensions in vocal tracts with acoustic reflection technology. They discovered that significant gender and racial differences exist in certain vocal tract dimensions. These findings will help researchers with a new anatomical database of those from different races and how their voice tracts differ for more study into it.

In this study, they measured volumetric differences in males from different races. They investigated vocal tracts, such as length differences in them, to see which would contribute to racial differences in acoustic characteristics. The findings help to support the hypothesis that those from different races may possibly have morphological differences when it comes to vocal tract dimensions. Those same dimensions could also be responsible for differences in vowel sound of specific dialect/speech.

People use  everything from their throats to noses when they speak, and since there are morphological differences there, one would reason that there would be differences in the voices between races, on average. Basically, those with different facial features should have different voices. Since the races have different facial features, as well as morphological differences in vocal tracts and larynx and everything in between, then there are obvious differences in voices.

Taking 50 blacks and 50 whites and having them say an ‘a’ sound which was then recorded. The researchers paired one black subject with one white subject and the individuals in the study were able to guess the correct race 60 percent of the time. The researchers then gave an acoustic analysis of the voices. What was then discovered was that all though the voices for the black subjects was within normal ranges, the black subjects had “greater frequency perturbation, significantly greater amplitude perturbation, and a significantly lower harmonics-to-noise ratio than did the white speakers.” The listeners were most successful in distinguishing voice pairs when the differences in vocal perturbation and additive noise were greatest (obviously) and least successful when those differences were minimal or absent (again, obviously). Since there was no fundamental difference in the mean fundamental frequency and format structure of the samples, it’s extremely likely that the listeners relied on spectral noise to differentiate black and white speakers.

Even blind people “see” race!! Yet more proof that the races differ in speech as well as have morphological differences between them.

I’ve always noticed that, on average, you can tell a black from a white and a white from an Asian. Testosterone also plays a part. In Rushton’s debate with Joseph Graves, he says that testosterone differences are the cause for racial differences in voice. Testosterone mediates a lot of things in the human body. Testosterone levels also mediate the deepness of an individual’s voice. Those with more testosterone have a deeper voice, and those with less testosterone have a higher voice. East Asians have the least testosterone out of the three races, and they have the highest-pitched voices. Conversely, blacks have the highest testosterone and have the deepest voices, as well as the most distinct voices between the races. Whites, as usual, fall in the middle.

Black males have a smaller overall size gradient, Asians the biggest, and of course, whites fall in the middle. The sound of voices doesn’t just vary between races, but by gender within races as well.

Can we “hear” race? The answer is yes!! Whether it’s morphological differences in the voice tract or larynx or  testosterone differences between races, we definitely can discern someone’s race on average when speaking to them. 

Ashkenazi Jews are not Khazar

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Many people in the alt-right say that “the Ashkenazi Jews are Khazar”. This is not true. This is based on an autobiography by a Jew who thought that if Europeans thought the Jews were European, they wouldn’t want to kill them. This is also based on one study, where all the rest of the literature says they derive from the Levant and the Middle East. I will go through the myth and then tell the truth of the origins of the Ashkenazi Jews.

In this research paper by Eran Elhaik, he says that the rise of European Jewry is explained by the rise of Judeo-Khazars. Though contribution of Khazar genetics can only be estimated by empirically, but the absence of genome-wide data precluded the Khazar hypothesis. The findings by Elhaik, he says, support the Khazarian hypothesis and it represents the European Jewish genome as an amalgamation of Caucasus, European and Semitic ancestry.

Razib Khan has this to say about it:

In general I have to say that the historical framework of the paper is very skeletal, verging on incoherent (at least to me).

Setting aside the historical fuzziness of the paper, the major issue I have is that though the methods are totally kosher, so to speak, the data you put into them strongly shape your outcomes. Dienekes and Maju both anticipated my own key concern. The “Middle Eastern” aspect of Ashkenazi Jewish ancestry might in fact be most well represented by populations in the zone of the northern Fertile Crescent and Eastern Anatolia; rather near or overlapping with the homelands of several of the Caucasian populations used in the above study as a proxy for Khazars. Additionally, modern Palestinians (the HGDP data set) are used as a reference to the Middle Eastern ancestors of Jews. I now believe that the Arabian contribution to the ancestry of Levantine and Iraqi Muslim population which dates to after the 7th century, and differentiates Muslim Arabs from their local non-Muslim Arab* co-ethnics, is significant. Perhaps on the same order of Germanic ancestry in modern England which dates to the 6th century and later. In plainer language the Caucasian component that is being detected in this paper may simply be a indigenous Middle Eastern ancestral element which has now been somewhat displaced northward in its modal frequency due to the expansion of the Arabs, and later the admixture of some Sub-Saharan admixture among Muslim Arabs.

Finally, despite the fact that I praise the author’s utilization of a wide array of contemporary statistical genetic methods, one can’t just do away with a thick and sturdy historical framework and reasonable questions derived from this superstructure.

And Dr. Kevin Macdonald’s thoughts on the matter:

The new findings were seen as support for the idea that there was significant admixture with non-Jews in Greco-Roman times. This is based on the clustering of the European/Syrian Jews and the fact that these groups have been separated since ancient times. The authors argue that the data are consistent with historical accounts of proselytism and large-scale conversions to Judaism in ancient times. When I reviewed the historical data in A People That Shall Dwell Alone (Ch. 4, pp. 62-78), I ended up rejecting this theory, coming down on the side of historians who doubted how important conversion really was. One thing that convinced me was that there was a lot of evidence for biases against converts. For example, once they converted they were regarded as very undesirable marriage partners and that a pure Jewish genealogy was a very big asset in the marriage market. Families keep their genealogies for generations, and there is a lot of evidence for hostility toward converts. Contrary to Atzmon et al., conversion is not required to explain the large numbers of Jews in the ancient world.

Though, this theory, before this one singular study came out, was first put forth by Arthur Koestler in his book The Thirteenth Tribe. He became interested in the founding of the Hungarian empire, and how the Khazars were at the center of that. He then makes a huge jump in logic to say that all of European Jewry are descended from those from Khazaria who then converted to Judaism.

This theory was quickly latched on to by the alt-right when it first was published and used as ammunition to say that the Jews weren’t the rightful bearers of Canaan (modern-day Israel/Palestine). However, we know that Jewish populations are more closely related to each other than to outside populations:

Livshits, Sokal and Kobylianskyt investigated the genetic affinities of Jewish populations. They concluded that Jewish populations are more like one another than they are to non-Jews and that pairs of Jewish populations from different locations are more alike than pairs of non-Jewish populations. They maintained that the most economical explanation of their findings is that the modern Jewish population throughout the world was derived from a common original gene pool which underwent few changes during the dispersion of the Jewish people. They also reported that it was highly likely that the common origin of the Jewish populations was more recent than that of the non-Jews.

Which, if Ashkenazi Jew were Khazar, we wouldn’t see this coming up in genetic testing.

Even the world’s foremost researchers on the Jews like Dr. Kevin Macdonald and Dr. David Duke say that the Khazar Hypothesis is long refuted.

In Ted Sallis’ article on the Occidental ObserverMore Jewish Genetics: The “Weak Khazar Hypothesis” he cites a study which says that there may be a minute component in the Ashkenazi Jewish genome which is Khazar, which that part is from a North Caucaus population. Though, that might just be showing genetic similarity and not that some of the Ashkenazi Jewish genome derives from those populations.

David Duke even accepted the Khazar theory as true for years as he admits, however, he says that it wasn’t until he thought of the hypothesis both scientifically and logically that his doubts on the theory became aroused.

He says that Koestler, who he didn’t know was a communist Jew, bragged in a Jewish magazine that he made the hypothesis to fight anti-semitism. He believed, and cited the Gospels as evidence, that if he could get Europeans to believe they are related by blood to Jews, that anti-semitism would be lessened. Dr. Duke then goes through many studies which show that, in fact, the Khazar hypothesis is long discredited.

In my own articles on this website, I have written about the origins of Ashkenazi Jews.

Jews migrated from the Levant to Rome and mated with beautiful Roman women which (partly) gave them their current intelligence.

A few thousand years ago, male Jews migrated from the Middle East and mated with beautiful Roman women who then converted to Judaism. The four major founders of the Ashkenazi Jew population have ancestry in prehistoric Europe, and not the Caucus or the Near East. The four minor founders share a deep European ancestry. So with genetic testing, we can see that the majority of the Ashkenazi population didn’t have its origins in the Caucus or Levant, but through assimilation of Roman women who converted to Judaism.

Male Jews migrated from the Levant to Rome during Greco-Roman times, which mass conversions led to 6 million Roman women who then began to practice Judaism. The genetic proximity of Ashkenazi Jews and Syrian Jews to Northern Italians, Sardinians and French populations suggest that there is non-Semitic ancestry in Ashkenazi Jews. The findings also say that any theories of Ashkenazi Jews having ancestry in Khazaria or from Slavs are incompatible with genetic studies. The close genetic similarity of Ashkenazi Jews and Southern Europeans has been noted in many studies.

So we have male Jews from the Levant who trekked to Rome around Greco-Roman times. They took beautiful Roman women as wives, who then converted to Judaism.

These two new studies from within the past few years again corrobarate that Ashkenazi Jews are not Khazarian, but derive from the same four founder populations; ancient European women and are not descended from Turkish populations.

Blogger Diversity is Chaos believes so. He says:

Persian Jews converted Turks to Judaism to create the rump of what would become today’s Jewish population, DNA research has revealed. The fascinating insight, which shows that most Ashkenazi Jews descend from Turkey, was made possible by state-of-the-art computer modelling and genetic techniques. The project, led by Israeli-born Dr Eran Elhaik, even pinpointed Iskenaz, Eskenaz and Ashanaz – three Turkish villages an ancient Silk Road route which still exist today – as part of the original Ashkenazi homeland.

As shown above, this is wrong. No idea why he wrote this article the other day, seeing as this debate has been put to rest for years.

He said that the word Ashkenaz likely derives from Ashguza, the ancient Assyrian and Babylonian term for Iron Age Eurasian steppeland people known as Scythians.

No. It is Biblical:

from modern Hebrew, from Ashkenaz, son of Japheth, one of the sons of Noah (Gen. 10:3).


Concurrent analysis of Yiddish suggests that it was originally a Slavic languagewhich the researchers think was developed by Jewish tradesmen travelling along the Silk Roads linking China and Europe 1,200 years ago.

The prevalent view claims Yiddish has a German origin, whereas the opposing view suggests a Slavic origin with strong Iranian and weak Turkic substrata,” they say. “One of the major difficulties in deciding was the unknown geographical origin of Yiddish speaking Ashkenazic Jews,” they say, but their analysis “demonstrates that Greeks, Romans, Iranians, and Turks exhibit the highest genetic similarity with Ashkenazic Jews”.

They show genetic similarity to those populations due to population migration. I have touched on and already linked to the origins of the Roman component in the Ashkenazi Jewish genome, and the same applies for those other populations. Genetic similarity does not mean that those populations were a founder population, or even that there is ancestry from those peoples.

Yiddish and modern German are both derived from the same source, which is Middle High German. Why, if they were Khazar, would it be derived from Middle High German? Why would the Ashkenazic travelers speak Old French, Hebrew and Aramaic? Yiddish is an amalgamation of languages with an extremely heavy German component. As the Jews traveled, they picked up new languages and began to integrate them into their language and eventually Yiddish formed.

To conclude, those who still believe and push the Khazar hypothesis are ideologically blinded. They let their bias cloud their judgement to the facts. Just because one singular study came out that says the Jews are Khazar is meaningless…. Since all other studies have shown that Jews, all Jews no matter where they live in the world, show affinities with the Middle East. Even the world’s foremost scholars on the Jewish people say that the Khazar hypothesis is wrong. One study on this doesn’t show that “all Jews descend from Khazars”, as we have to take a look at all studies as a whole and see where they point. All studies do not point to an origin like this, so it’s safe to say that this one study be thrown in the trash where it belongs. It’s intellectually dishonest to believe the Khazar hypothesis when it has been discredited time and time again by the newest genomic studies.

In Defense of Jason Richwine

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I came across two articles today, one from The Atlantic and the other from judgybitch.com. Both have attacked Jason Richwine’s dissertation in which he calls for a change to the US immigration policy to turn away low IQ immigrants and only accept high IQ ones. I agree fully with this (if it’s completely controlled, of course). This would drop crime as well as save us more money in welfare and other government programs that low IQ peoples take.

By 2050, 9 out of 10 people in the US will be obese or overweight and by 2020 80 percent of US men will be obese or overweight. This is due, in part, to an influx of those with lower IQs from South of the Border. Jason Richwine’s argument for testing immigrants will, in turn, lower obesity rates in America.

Dr. James Thompson noted how continued mass immigration from the South of the Border would decrease IQ, this is a real and pressing issue. A country is only as good as its majority population and by allowing all of these low IQ people into the country, our country will transform into theirs, which is ironic since that’s the exact thing they’re running away from. You cannot run away from genetics. The overall ‘Hispanic’-white gap is 10.2 points or .72 SDs. That will lower the average IQ of the country even more, and in turn, give us all a lowered quality of life. The average IQ of Mexico is 88 (Lynn and Vanhanen, 2002) so by allowing unfettered mass immigration without checking average IQs to see if they’ll be of any use to us as a country will lead to eventual irreversible effects if this isn’t stopped soon.

The first article I’ll look at is the one from The Atlantic:

Let’s start with the fact that there is no such thing as a direct test of general mental ability. What IQ tests measure directly is the test-taker’s display of particular cognitive skills: size of vocabulary, degree of reading comprehension, facility with analogies, and so on. Any conclusions about general mental ability are inferences drawn from the test-taker’s relative mastery of those various skills.

IQ tests test g or the general intelligence factor which encompasses all mental abilities. I guess the author of this piece has never heard of Raven’s Progressive Matrices. It’s a ‘culture free’ IQ test where the test is based on pattern recognition. No bias there.

Even then, if they don’t speak English and speak Spanish, they can get tests in their native language which are not biased. Gottfredson (1994) and 51 other eminent intelligence researchers signed a 25 point statement in which one of the statements was:

Intelligence tests are not culturally biased against American blacks or other native-born, English-speaking peoples in the U.S. Rather, IQ scores predict equally accurately for all such Americans, regardless of race and social class. Individuals who do not understand English well can be given either a nonverbal test or one in their native language.

They will be given the nonverbal test (RPM, see below) or one in their native language, which still test the same underlying concept of the general intelligence factor.

They found that being raised by high-SES (socioeconomic status) parents led to an IQ boost of between 12 and 16 points – a huge improvement that testifies to the powerful influence that upbringing can have.

False. See below.

A study of twins by psychologist Eric Turkheimer and colleagues that similarly tracked parents’ education, occupation, and income yielded especially striking results. Specifically, they found that the “heritability” of IQ – the degree to which IQ variations can be explained by genes – varies dramatically by socioeconomic class. Heritability among high-SES (socioeconomic status) kids was 0.72; in other words, genetic factors accounted for 72 percent of the variations in IQ, while shared environment accounted for only 15 percent. For low-SES kids, on the other hand, the relative influence of genes and environment was inverted: Estimated heritability was only 0.10, while shared environment explained 58 percent of IQ variations.

Turkheimer was right that he did find gene x environment interactions that made genetic influences weaker and shared environment stronger for those from poorer homes in comparison to those from more affluent homes. Though most studies show no interaction effects, or interactions vary significantly.

Other studies have shown that heritabilities are the same both within as well as between white and black samples. That led Jensen to label this the ‘default hypothesis’. Researchers analyzed full and half siblings from the NLSY on three Peabody Achievement Tests. 161 black full siblings, 106 pairs of black half siblings, 314 pairs of full white siblings and 53 pairs of white half-siblings. with measures in math and reading. The best fitting model for all of the data was by which the sources of the sources of the differences between those within race and the differences between races were the same, at 50 percent genetic and environmental. The combined model (50/50) best explains it, whereas the culture-only and genetics-only models are inadequate.

IQ tests are good measures of innate intelligence–if all other factors are held steady.

This is wrong. IQ tests are fine all around the world. RPM is one of the best out there and correlates with g between .8 and .9.

But if IQ tests are being used to compare individuals of wildly different backgrounds, then the variable of innate intelligence is not being tested in isolation. Instead, the scores will reflect some impossible-to-sort-out combination of ability and differences in opportunities and motivations. Let’s take a look at why that might be the case.

Intelligence – g – is the same across every population in the world.

Comparisons of IQ scores across ethnic groups, cultures, countries, or time periods founder on this basic problem: The cognitive skills that IQ tests assess are not used or valued to the same extent in all times and places

This is why they get re-standardized.

Indeed, the widespread usefulness of these skills is emphatically not the norm in human history. After all, IQ tests put great stress on reading ability and vocabulary, yet writing was invented only about 6,000 years ago – rather late in the day given that anatomically modern humans have been around for over 100,000 years. And as recently as two hundred years ago, only about 15 percent of people could read or write at all.

Doesn’t matter. See Raven’s Progressive Matrices above. The general intelligence factor is the same in all populations around the world. There are ways to give intelligence tests, such as RPM, to those who don’t read or write.

More generally, IQ tests reward the possession of abstract theoretical knowledge and a facility for formal analytical rigor.

Abstract thought is linked with intelligence. Those with higher IQs are more analytical than those with lower IQs.

To grasp how culturally contingent our current conception of intelligence is, just imagine how well you might do on an IQ test devised by Amazonian hunter-gatherers or medieval European peasants.

I touched on this in my refutation of Robert Sternberg. The concept of does not change over time. The more intelligent you are, the better chance you’ll have to survive in those places.

Such skills are used more intensively in the most advanced economies than they are in the rest of the world. And within advanced societies, they are put to much greater use by the managers and professionals of the socioeconomic elite than by everybody else. As a result, American kids generally will have better opportunities to develop these skills than kids in, say, Mexico or Guatemala. And in America, the children of college-educated parents will have much better opportunities than working-class kids.

Those skills are used much more in advanced economies because of higher average innate intelligence. The children of college-educated parents have much better opportunities than working-class kids because intelligence is strongly linked to socioeconomics status.

Among the strongest evidence that IQ tests are testing not just innate ability, but the extent to which that innate ability has been put to work developing specific skills, is the remarkable “Flynn effect”: In the United States and many other countries, raw IQ scores have been rising about three points a decade. This rise is far too rapid to have a genetic cause. The best explanation for what’s going on is that increasing social complexity is expanding the use of the cognitive skills in question – and thus improving the opportunities for honing those skills.

Let’s say Flynn is right. The average black now is as intelligent as the average white in 1945. That’s supposed to show that the race difference in IQ is environmentally caused because there hasn’t been that much genetic change in the white population and the IQ has allegedly gone up 15 points. So, you can have a 15 point difference created by just an environmental change, no one knows why. Some think better nutrition or malnourished brain, etc. That’s also a fallacy. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. The Flynn Effect make’s that highly unlikely and here’s why.

The Flynn Effect, assuming it’s real, has been acting completely uniformly in every population. Any country you ask, the rate of increase is 3 per decade. That means it’s an environmental factor that affects whites and blacks the same way as well as the whole world. And as a result of this uniform environmental factor, you have a difference in IQ that’s being preserved. That would suggest that the response on the parts of blacks and whites is due to some non-environment factors, a genetic factor, which is making the difference in IQ remain constant as the Flynn Effect goes into effect.

What makes it even more unlikely, in the last 60 years, their environments have become very similar since segregation. These differences don’t exist now, they go to the same schools by court order, same TV shows, same movies, basically same environment for both, and yet, that increasing similarity in the environment, the Flynn Effect, the IQ gap has remained intact. Which means whatever counts for the gap is genetic and not environmental. The more and more similar the environment, the less and less of the difference can be due to the environment and the more and more it must be due to genes. So this 15 point gap surviving these changes in the environment, seems more and more likely to be genetic in origin.

So because this ‘Effect’ is the same across all populations and the gap didn’t close, that means it’s genetic. If the gap persisted even when IQs were rising 3 points per year, the B-W gap has still persisted, proving that it’s genetic.

That is why the Flynn Effect is irrelevant. This “Effect”, has been a slight upward trend in IQ, around 3 points per decade, which, in my opinion, has to do with the advent of better nutrition and an industrialized society. The rise in IQ started around 1880, almost perfectly coinciding with the industrial revolution in America. Along with a more industrialized society, it’s possible to give most citizens in the country good enough nutrition to where they are not iodine deficient (adding iodine to our salt boosted Americans IQs), as well as being deficient in zinc, iron, protein and certain B vitamins which the effects of not getting enough leads to the brain not growing to its full potential, which in turn leads to a lower IQ.

One more point on the Flynn Effect. The Flynn Effect does not occur on g, as it is not a Jensen Effect. Rushton defines Jensen Effect as follows:

Significant correlations occurring between g-factor loadings and other variables have been dubbed “The Jensen eff€ect”.

Thus the secular increase in test scores (the “Lynn±Flynn e€ffect”) is not a “Jensen e€ffect” nor is this the first time the discriminating power of the Jensen eff€ect has been shown.


The Flynn effect is acutely embarrassing to those who leap from IQ score differences to claims of genetic differences in intelligence.

Not at all, since it’s easily explainable by better nutrition since the beginning of the industrial revolution. It’s also not even on so why this gets discussed is beyond me.

Specifically, it is based on the ahistorical and ethnocentric assumption of a fixed relationship between the development of certain cognitive skills and raw mental ability. In truth, the skills associated with intelligence have changed over time–and unevenly through social space–as society evolves.

The relationship exists and there is a strong correlation between cognitive skills and raw mental ability. More intelligent people have better functioning societies than less intelligent people. This is an objective fact.

But contrary to the counsel of despair from hereditarians like Richwine, those deficits aren’t hard-wired. Progress in reducing achievement gaps will certainly not be easy, but a full review of the IQ evidence shows that it is possible. And it will be aided by policies, like immigration reform, that encourage the full integration of Hispanics into the American economic and cultural mainstream.

Jason Richwine is correct. Progress in achievement gaps will not close, barring the continued dysgenesis that America is facing. Immigration reform will not change anything. They don’t want to assimilate; they want to come and leech off of our Welfare State. The denial of genetics and scholastic achievement won’t be able to be held for long. In this study in which Robert Plomin was one of the researchers, it was found that 60 percent of the difference  between individual 16-year-old students in the UK could be attributed to genetic factors. We know that IQ is linked to academic achievement and since that’s heritable as well, we will soon see that race and ethnic differences in IQ and academic achievement are, without a shadow of a doubt, are real and do not exist because of any economic deprivation or some other kind of non-biologic factors.

For the second article, from judgybitch.com, in which she only says one correct thing in it and it’s:

Here’s a little pet theory of mine I’d like to throw out, just for the hell of it.  I think humans prefer lighter skin and hair and eye colors because those tend to be the result of recessive genes.  A man with darker tones who has a child with a woman of lighter tones will almost always see his genes expressed in the children.  Dark tones tend to be dominant.  The preference for lighter skin is a natural paternity test.

This is called sexual selection, which is natural selection which arises for selection of traits in the opposite sex. Selecting for certain traits which the opposite sex found appealing, for example, is how long hair got sexually selected for outside of Africa along with selection for hair, eye, and skin color. Selecting for these traits had them become more prevalent and they eventually stayed due to intense selection for them.

For example, Eurasian women got selected for beauty and Eurasian men who got selected for intelligence as men had to be more intelligent in order to hunt for food. Conversely, African women gathered and hunted for food and became slightly more intelligent than African men who became the more attractive sex (Fuerle, 2008).

But other than this she is wrong.

You know what IS linked very strongly to lower IQs?

Malnutrition.

http://www.sciencedaily.com/releases/2004/11/041117005027.htm

http://www.ncbi.nlm.nih.gov/pubmed/2628311

http://www.nature.com/pr/journal/v5/n11/abs/pr1971371a.html

The idea is not even the slightest bit controversial.  Children who are starved, especially in the earliest years of life, perform very poorly on IQ tests compared to peers who received adequate nutrition.  Like, really poorly.  IQ’s down around 60 (100 is average).

Let’s look at this world hunger map, shall we?

p1_hunger_map-1.jpg

http://www.geographictravels.com/2008/07/world-hunger-map.html

Oh well now, would you look at that.  Looks like it’s mostly black and Hispanic folks who are starving.   And all those white folks are living life to the hilt, with full bellies and bright futures.

Must be a coincidence.

It’s not a coincidence. There is no coincidence that if you superimpose an IQ map over the world hunger map, that a super majority of the low IQ countries would have bad nutrition and be starving, whereas those higher IQ populations would have better nutrition and, therefore, higher IQs and lack of malnutrition and starvation. There are environmental factors involved in this, which I have gone through in my article IQ, Nutrition, Disease and Parasitic Load. Yes, those environmental variables decrease IQ; but in the case of Africa, if their full genotypic IQ were expressed in their phenotype, they would have an average IQ of 80, 9 points away from the lowest average European country which is Serbia at 89. They would then be able to have better functioning societies and not have to rely on outside aid. Though, their low IQs are the cause of evolution, those factors only cause about 10 points of difference (depending which of the variables I mentioned exist in those areas).

Let’s look at this map of food insecurity in the United States:

091117-food-foodinsecurity.png

http://www.nextgenerationfood.com/news/food-insecurity-in-the-us/

Highest rates of food insecurity:

Mississippi

Texas

Arkansas

Lowest rates of food insecurity:

North Dakota

Massachusetts

Virginia

Gosh, I wonder where all the black and Hispanic people are?  North Dakota, right?

According to the USDA, in a report titled Household Food Security in the United States in 2011, black and Hispanic families are more than twice as likely to experience food insecurity as white families (p. 11).

White                    11.4% of families food insecure

Black                      25.1%

Hispanic               26.2%

http://www.ers.usda.gov/media/884525/err141.pdf

Gosh, I wonder where black and ‘Hispanic’ people are? Mississippi, Texas, and Arkansas right? What is the cause of the food insecurity? Lower intelligence. What is lower intelligence highly correlated with? Obesity.

If you keep in mind the fact that obesity (especially as the result of heavily processed, nutrient deficient junk foods) is also a form of malnutrition, it seems to me that there is an entirely different explanation for why certain racial groups might tend to perform lower on IQ tests.

Sure it is. A big cause for obesity is lowered intelligence (Kanazawa 2007). What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ.  The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This clearly shows that those obese individuals who score low on IQ tests, more often than not, are obese because of their intelligence. The lack of ability to delay gratification is also correlated with low IQ (Mischel and Metzner, 1982).

Becoming obese is largely in part related to environmental factors, but there are correlates with obesity and genetic factors, as well as racial and ethnic differences in obesity, which are due, in part, to environmental as well as genetic factors. All of these factors fall back to a) lower intelligence, b) differing physiology and c) differing nutritional habits. Lower IQ is the main reason, though, for these differences which manifest itself as differences in scores of cognitive ability. Those with lower scores than have higher chances of having negative effects in life, such as low SES, higher chance of becoming obese and so on.

Correlation is not causation.

This is the liberals word phrase they use when they cannot contest data and know it so use the same old boring phrase. When you get the same result over and over using the scientific method, then it’s safe to say that the same results and conclusions that get brought up time and time again are real and cannot be explained away by the correlation does not mean causation line.

And furthermore, I haven’t read Richwine’s dissertation, nor do I plan to, so I don’t know if he offered any tentative explanations for his findings.

Didn’t even read it and is giving a critique of it. How does that work?

It looks to me like Richwine is a gigantic racist asshole, because he is using his findings to try and limit the opportunities for Hispanic people to come to the United States, because dumb spics.

Lower IQ people commit more crimes than do higher IQ people. This phenomenon is well-noted that those with lower intelligence commit crime, as the average IQ of a criminal in America, is 85, whereas the average IQ for a juvenile is 92. The average juvenile IQ is higher because more often than not, those who are habitual offenders in childhood become habitual offenders in adulthood, and at adulthood IQ drops from childhood where the environment was able to artificially boost their IQs.

What if I’m right?  What if IQ differences are traceable to malnutrition?  That would indicate a whole different set of interventions and policies than just turn them away.

You are part right, but that won’t put any big dent in any genetic/phenotypic IQ differences and still, mass immigration from South of the Border still wouldn’t be OK in the first place.

In shutting down the conversation about race and IQ, Harvard students are explicitly saying they don’t WANT to find a reason behind low performance on IQ tests amongst certain racial groups.  They don’t CARE why some groups are not reaching their full human potential.  They don’t give ONE SINGLE FUCK about anyone other than themselves. It could be as simple as making certain children have access to proper food and nutrition.

I at least give her credit for acknowledging the biological reality of race and the reality of IQ. But she thinks that malnutrition plays too big a part in the ethnic IQ gap than it does in reality.

As I have covered here before, people will do anything they can to deny the validity of IQ tests. However, their explanations cut it.

People who attempt to deny biological differences in intelligence because they strongly predict positive life outcomes will do anything to deny their validity. But that doesn’t change how strong a predictor they are in regards to predicting both positive and negative successes in life.

Those who attempt to deny any differences between races, like Chanda Chisala (I know you can see this Chanda, still waiting for a response to the criticism of your horrible article that “redneck genes” are the cause for the black-white IQ gap), who are wrong in their premises on the cause as well as how to fix the gap. They will do anything to attempt to explain away a gap which is, at least, 50 percent genetic in origin.

The attack on Jason Richwine is because, of course, he’s right. They don’t want to admit he is right so they do whatever they can to discredit his argument, by calling him a ‘racist’. But that doesn’t negate his data, and as seen above, any arguments against Richwine’s dissertation are unfounded.

Germany is going to begin IQ testing their immigrants, why can’t we?

Differential K Theory, GFP, and the Evolution of Conscientousness

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There is a link between higher IQ and higher ability to be more conscientiousness, which is then linked to the GFP or General Factor of Personality. Two meta-factors were identified beyond the Big Five Personality Traits and were described as ‘Plasticity’ and ‘Stability’ (Deyoung et al, 2002). To quote from the paper:

Stability subsumes Conscientiousness, Emotional Stability (the reverse of
Neuroticism), and Agreeableness, and refers to the extent to which
an individual is consistent in motivation, mood, and social interac-
tions. Plasticity encompasses Extraversion and Openness to experi-
ence, and refers to the extent to which a person actively searches
for new and rewarding experiences, both intellectual and social.

Why did this evolve, especially so closely with high intellect? It evolved due to conscientiousness, which is defined as being thorough, careful, and vigilant.That, coincidentally enough, being needed to survive the harsh winters of Northern Europe and Siberia. Higher conscientiousness was is also another reason for the formation of European societies. With being able to be more conscientious, this, along with genetic pacification, is yet another cause for the cucking of Europe.

When our ancestors trekked out of Africa and into Siberia and Northern Europe, they needed differing abilities than those peoples who stayed in the more tropic climates. Those in the tropics, for the most part, could just lounge around all day. With food being readily available, there was really no pressing need to “save” or “partition” their findings (as Africa is full of mostly a hunter-gatherer societies). Conversely, in Europe and Asia, with harsh conditions in regards to their environment, which made food less plentiful than in the tropics, this meant that more cooperation was needed. Due to more cooperation being needed to survive, planning ahead (abstract thought) evolved to better help cope with the harsh environment.

The aforementioned factors in Europe and Asia then led to the higher rates of altruism seen today. Ancient Europeans needed to be thorough, vigilant and careful. Whether they needed to be careful with food storage, how much to eat, whether or not to help someone, etc, it’s clear that conscientiousness evolved with higher intelligence. Since higher intelligence is correlated with those three things involving conscientiousness, they evolved hand in hand, as selection only selects for good traits and discards the ones that aren’t useful.

These two environments that the three races evolved in then set the stage for what’s going on today. With Africans’ lack of conscientiousness, this leads to them not being vigilant, careful or thorough. This can be seen with how sloppy they are when they commit crimes. Their ancestral environment wasn’t conducive to conscientiousness, and in turn, higher IQ, so they evolved without the need of conscientiousness, as their societies (for what they are), function ‘well’ in their perception. This is yet another reason why that we cannot live together. Differing evolutionary strategies lead to these causes, yet we still think we can acclimate some peoples into society when their biology says otherwise.

JP Rushton proposed that the GFP (General Factor of Personality) and IQ were linked. It was found that the correlation between the GFP and IQ was -.23. The higher the score, the higher the individual scores on the GFP. He noted that the correlation is so low, possibly due to the restricted range of the sample. Rushton provided an argument for the evolutionary process of cognitive ability and personality evolution. This is clear evidence of the GFP and IQ evolving hand-in-hand.

Lacking a high IQ, and therefore, lack of g, Africans (as well as other colored peoples), on average, have lower g and therefore lower conscientiousness, which then is a huge cause for crime. Increases criminality has been correlated, like I’ve said here before, to a lower verbal intelligence. Though this higher IQ and higher GFP is being taken advantage of. Ever since that fateful day in 1964, white pathological altruism has been taken advantage of. Those with lower conscientiousness know they can take advantage of those with higher IQ and higher conscientiousness as altruism is correlated highly with IQ and conscientiousness.

There is an altruistic personality; the altruist has a high IQ, is conscientious, and altruistic. Those on the opposite end of the spectrum, however, take advantage of that and this can be seen with the political climate around the world in regards to other races’ feelings towards whites.Conversely, those who are r-selected and have a low IQ and GFP tend to be more hostile and commit acts of aggression. This multiculturalism due to the altruistic personality on a large scale is one of the reasons for the mass immigration into Western societies. People, as a whole, become collectively altruistic. Then, those lower IQ, lower GFP, r-selected people then take advantage of the more altruistic people. They then turn into a parasitic entity, sucking the host dry before moving on to their next victim.

This is where a high GFP does not work, in multicultural societies. Of course, this is also due to ethnic dissimilarity, but the other thing I brought up along with that ethnic dissimilarity are all of the negative effects of those that are r selected, which, in their own societies is ‘fine’, but to who are K-selected and have complex societies, those behaviors are archaic.

There is a high correlation between low IQ, low conscientiousness, archaic actions, lack of abstract thought, and lack of society building. We know that those with lower IQs commit more crime on average than those with higher IQs.

This is why allowing non-Western people who are abnormal to our societies  is a bad move, since they don’t share the same evolutionary track, and therefore, due to differing selections due to evolution, evolved differing behaviors to better adapt to the climate, environment, and surroundings.

Since skin color and IQ correlate at -.92, meaning the darker the skin the lower the IQ and vice versa, this is yet another great assessor on whether an individual has a high IQ, and is, therefore, conscientious. This is due to, as I alluded to earlier, the environment in sub-Saharan Africa being conducive to lack of ability to delay gratification. Due to that, we can infer, on average, whether someone will be conscientious or not. Since their ability to delay gratification is impeded due to certain evolutionary pressures not put on Asians and Europeans, they will, therefore, be less conscientious, which is a crucial building block in maintaining a successful society.

To quote Templer from his memorial paper dedicated to Rushton on the different correlates with skin color and different environments/effects:

The research of Templer and Arikawa (2006) supports Rushton’s contention that higher intelligence develops in colder climates. They used 129 countries with primarily indigenous populations (Asia, Africa, and Europe) and correlated culture fair IQ (Lynn & Vanhanen, 2002) with temperature. In addition to temperature, Templer and Arikawa used skin color provided by an anthropology book (Biasutti, 1967). IQ correlated .92 with darker skin color, .76 with winter highs, .66 with winter lows, and .63 with per capita income. Previous research by Meisenberg (2004) reported a correlation of .89 between skin reflectance and IQ in a similar study. Templer (2010b) found a correlation of .96 between skin color measure used by the Templer and Arikawa and the one by Meisenberg’s skin reflectance. Because both measures were independently determined using different methodology, they both can be regarded as highly valid measures of skin color.

The cause of these two variables being correlated is evolution. They paired well with each other, so over tens of thousands of  years, they got selected for with each other and persisted to today. Since we have modern societies and are much more civil (some of us), we can better see these differences in personality as well as behavior. There are This General Factor of Personality was able to evolve due to evolution in cold climates. The altered intelligence, which then altered personality. This r/K Life History Theory of Rushton’s blend’s beautifully with the GFP and intelligence. Evolution in cold climates along with genetic isolation caused differing evolutionary trajectories for each race/ethnicity which led to differences in crime, IQ, socioeconomic statussexual maturitycultures, and so on. There are clear genetic differences brought on by the environment (due to evolution), which leads to  differing societies based on differing evolutionary trajectories. Conscientiousness and intelligence, the whole General Factor of Personality, evolved in Northern populations since it was more beneficial in that environment, and to survive, this is what done to adapt to the environment through natural selection, which then led to racial differences.

Germany Begins to (Slightly) Wise Up: Will Begin IQ Testing “Migrants”

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Haaretz reported today that Germany was going to begin IQ testing on the ‘migrants’ to assess where talent and what occupational groups that they could put them in. This is a slightly positive change with all of the negativity this past year.

The mean IQ of Arab countries is 84 (Templer, 2010). With around 1.2 million ‘refugees’ coming from land and sea, assuming a SD of 15 (seeing as Arabs are Caucasian, I’ll assume a SD of 15), 50 percent of them fall at or below 84. So 600k at 84 or below. 16 percent fall at 100. 192k fall at 100. 12k at 120 and 1,680 fall at 130. 50 percent fall below 84. In America the average IQ for a repeat criminal is 85. With an IQ of 85, you can see that criminality begins to increase. This is due to lack of abstract thought(linked to verbal ability), which has them not think of the consequences of their actions before they act. At or below 85 is 1 in 6, 68% of the population is within 1 SD of 100, and 2.5% of people are 130 or more.

I can’t find any data on Arab testosterone at the moment, so I’ll just assume that it’s higher than Europeans due to the Arabs’ closer proximity to the equator (someone correct me if I’m wrong), as that’s why African’s testosterone is high. Due to higher average testosterone combined with low IQ, this leads to increased aggression along with increased sex crime, which is a cause for some of the sex assaults on European women by Muslim men. I can’t find anything on terrorist IQ, the closest I can find is how the FBI convinced a man with an IQ of 51 to attempt terrorist acts, though that’s an extreme case. Since low IQ is correlated highly with lack of abstract thought, it was easier for him to become convinced to do it. Like in most organizations, the more intelligent ones are at the top so they tell the lower IQ ones what to do. Though, by administering these tests, they will greatly lower their chances for another terrorist attack, seeing as those actions are correlated with low IQ.

In a study on prison inmates, IQ predicted inmate misconduct. Using a sample of 2500 inmates over 30 institutions from August 2004 to June 2006, it was found that those inmates who had higher IQs were involved in fewer incidents as well as being less likely to commit violent behavior. Verbal intelligence has been posited to be some of the cause for increased crime, seeing as verbal IQ is correlated with delinquent behavior, which is due to lack of abstract thought being correlated with lower IQ. With higher testosterone being correlated with low IQ and increased androgen sensitivity along with higher sperm counts (both are indicators of higher testosterone) being correlated negatively when measured by speed of neuronal transmission which causes a trade-off between g (general intelligence) and neuronal transmission, this shows that increased testosterone means decreased IQ. This is also seen with how higher IQ people have a lower sex drive.

I did say in my article Non-Western People are Abnormal for Our Society, that, as the title says, non-Western people are abnormal for our society due to not sharing our cultural values, which, we know is genetic. Though, higher IQ individuals will be better able to acclimate into society, as well as have a decreased proclivity to commit crime.

Since there are some evoultionary reasons for suicide bombings due to increased inbreeding this increased genetic similarity between them which led to increased altruism due to genetic similarity, by allowing those with higher IQs, this will lead to a greatly increased chance for attacks to happen as higher IQ people are better at controlling impulses.

This is a move I agree with. All countries should implement this procedure (obviously not enough to where it begins to displace the native population). With there being a cut-off limit on IQ, lets say 105 or even 110, that guarantees a high chance of those who are immigrating will be of value to the country and bring something to the table instead of the current situation with the benefits they currently receive (and lets be honest, you know these rules aren’t being followed). So by implementing this policy not only in Germany, but around the world, this would be a great thing for the West, to restrict immigration only to high-skilled workers, with a background check, intelligence test and someone with good credentials. Of course, only in sectors that really need the help. I of course advocate for the natives of any country to have first dibs when it comes to getting a job.

All in all, this is good move because a) rapes will be lessened and b) there won’t be as much individuals on welfare because there will be an (assumed) moratorium on those with lower IQs, leaving the higher IQ ones to find jobs and contribute to the economy.

Remember the last time Germany used IQ tests? =^)

Smoking and Race

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From the brands of cigarettes people use to the types of cigars people use, there are variations by race. There are also death rate differences and variations in how peoples of different race and ethnicity. I will explore causes for these points as well.

From the CDC’s Fact Sheet on tobacco use, we can see that Marlboro (41 percent), Newport (12 percent), Camel (8 percent), Pall Mall (8 percent) and Pyramid (2 percent) were the leading cigarette brands.The percentage of those older than 12 years old who smoked menthol was 19.1% black, 3.6% Asian, 7.8% ‘Hispanic’, and 6.5% white. You can see this looking in any majority black area how younger blacks most always smoke menthols, mainly Newport and sometimes Kools.

In my experience, that has been the case. For whites, the main brand was either Marlboro menthol, Marlboro lights or Marlboro Reds. For Asians it was most always Parliament Lights; they sure do love those.

Exposure to Newports in their environments may also be a factor for blacks smoking more menthol cigarettes, such as Newports. I have already written a bit about the media’s involvement in both a positive and negative way that affects behaviors, so by seeing more advertisements for a certain kind of cigarette, they’ll be more likely to smoke the brand that they constantly see, see their parents or siblings smoking (though, controlling for that in the study, they were still able to recognize Newports) smoking or ones that they can take that are lying around. Regardless of race, those students who were able to recognize Newports were more likely to begin at follow up even after controlling for other risk factors. In this sample of 1179 students (this was a longitudinal study), non-recognition of Camel and Marlboro did not predict smoking at follow-up.  These factors also involve what I will discuss below.

Caraballo (1998) found that serum cotinine levels were higher than blacks than they were in whites. That is, blacks have higher levels of the metabolized form of nicotine in their bodies than do whites called ‘cotinine‘. This causes blacks’ bodies to absorb more nicotine than whites due to these biological factors. This may possibly explain why blacks have more cases of lung cancer and are less likely to quit smoking.

Non-‘Hispanic’ blacks also have two times the amount of cotinine than do Mexican and white Americans. This affects how much of the nicotine absorbed into the blood stream as well as the increase in getting cancer.

The differences in cancer disparity between blacks and whites cannot be explained by the preference for a certain brand of cigarette. Though, that study does confirm that those who smoke more mentholated cigarettes take deeper inhales. So in a way, in can be said to be explained by brand preference, since those who smoke menthol cigarettes inhale more deeply than those who smoke a non-mentholated brand.

Ross et al (2016) discovered that blacks take more pulls per cigarette and take deeper, longer pulls than do whites, which is the cause for the disparity in lung cancer between blacks and whites (along with higher cotinine levels in blacks, that’s the cause for more nicotine absorption). Deeper inhales means more nicotine is being absorbed into the body and therefore cotinine levels increase.I could also see personality differences playing a factor in who takes longer pulls and more pulls of a cigarette as well.

Higher testosterone levels may also be correlated with lung cancer. With blacks having more testosterone on average than whites, we can see how these disparities in  hormone levels between the races are the cause for differences in acquisition of disease rate between the races. It seems that all cancers have high correlations with increased testosterone, not just prostate. Higher testosterone is associated with many negative variables, and of course, blacks have some of the most negative health effects. This is a combination of genes x environment. Their environment is more conducive to menthol cigarettes (mostly Newports), blacks also are more extroverted, which means they’re more sociable and therefore can coerce each other to do things, such as smoking (lower IQ also plays a part in coercion).

In teenage populations, whites showed a higher use for tobacco smoking and marijuana usage, but in the 20s, blacks and ‘Hispanics’ are more likely to pick up the habits, while whites drop off. The researchers conclude that we need to better understand why these substance abuse behaviors exist, which differing personality traits (due to testosterone, as well as that being a factor for smoking more) are part of the cause for it in my opinion.

Higher free and total testosterone was found in males, even after stratification of age, BMI, triglycerides and alcohol consumption were controlled for. This shows why more blacks and ‘Hispanics’ are represented more in  the statistics after age 20, as that’s when genetics takes full effect, so they would be over-represented in these cases.

With the higher natural cotinine levels, this causes blacks to absorb more nicotine; they take more pulls per cigarette as well as deeper pulls. Along with smoking cigarettes with more nicotine and more tar in them, this is a cause for the disparity between blacks and whites and how it involves the acquisition of lung cancer. Higher testosterone individuals turn to smoking more than lower testosterone individuals.

I theorize that part of the reason for deeper pulls of a cigarette as well as more pulls is correlated with the amount of testosterone one has, which is then correlated with how extroverted they are. Extroversion leads to being around others more often, which, even with desegregation, there has been less integration, not more. Since they’re more likely to be around each other due to desegregation not ending people segregating by race, they then are exposed to others who are smoking as well as doing other thing that younger children with higher testosterone will be more likely to do, in part because of exposure to the new stimulus along with higher testosterone which leads to more impulsive behavior.. This leads to one of many social and biological variables that lead to blacks having higher rates of lung cancer due to smoking.