Ethnic origins of Forbes world billionaires (2013)

The ethnic breakdown I come up with for the March 2013 update of Forbes' "The World's Billionaires" list:

No. %
Northwestern European 415 29.10
Asian or Pacific Islander 313 21.95
Jewish 249 17.46
Middle Eastern or Central Asian 120 8.42
Eastern European 95 6.66
Southern European 84 5.89
(New World) Hispanic or Brazilian 75 5.26
South Asian 69 4.84
Black 6 0.42
total 1426 100

Particularly for Eastern Europe, individual classifications may be less accurate than my classifications of US billionaires, but the overall breakdown should be reasonably close to reality. I may have incorrectly included a few people in the Jewish list, but if anything probably incorrectly left off a larger number -- my Jewish category should be more accurate/comprehensive than Forbes Israel's "Richest Jews" list in any case. Note that I've arbitrarily chosen to include Tatars in the Middle Eastern category, along with Armenians, Azerbaijanis, etc. Mongoloid-appearing Kazakhs were included in the Asian category. I generally put Latin Americans with Northern European or Italian names (who were not obviously mestizo) in the appropriate European category.

You're free to post any corrections.

Related posts:

Full list below.

Neolithic mitochondrial haplogroup H genomes and the genetic origins of Europeans

Making of Europe unlocked by DNA
But, from the Middle Neolithic onwards, DNA patterns more closely resembled those of people living in the area today, pointing to a major - and previously unrecognised - population upheaval around 4,000 BC.

Co-author Prof Alan Cooper, from the University of Adelaide in Australia, said: "What is intriguing is that the genetic markers of this first pan-European culture, which was clearly very successful, were then suddenly replaced around 4,500 years ago, and we don't know why.

"Something major happened, and the hunt is now on to find out what that was." [. . .]

A significant contribution appears to have been made in the Late Neolithic, by populations linked to the so-called Bell Beaker archaeological culture. Sub-types of haplogroup H that are common today first appear with the Beaker people and the overall percentage of individuals belonging to the H clan jumps sharply at this time.

The origins of the "Beaker folk" are the subject of much debate. Despite having been excavated from the Mittelelbe Saale region of Germany, the Beaker individuals in this study showed close genetic similarities with people from modern Spain and Portugal.

Other remains belonging to the Late Neolithic Unetice culture attest to links with populations further east.

"We have established that the genetic foundations for modern Europe were only established in the Mid-Neolithic, after this major genetic transition around 4000 years ago," said co-author Dr Wolfgang Haak.

"This genetic diversity was then modified further by a series of incoming and expanding cultures from Iberia and Eastern Europe through the Late Neolithic."

Neolithic mitochondrial haplogroup H genomes and the genetic origins of Europeans
Haplogroup H dominates present-day Western European mitochondrial DNA variability (>40%), yet was less common (~19%) among Early Neolithic farmers (~5450 BC) and virtually absent in Mesolithic hunter-gatherers. Here we investigate this major component of the maternal population history of modern Europeans and sequence 39 complete haplogroup H mitochondrial genomes from ancient human remains. We then compare this ‘real-time’ genetic data with cultural changes taking place between the Early Neolithic (~5450 BC) and Bronze Age (~2200 BC) in Central Europe. Our results reveal that the current diversity and distribution of haplogroup H were largely established by the Mid Neolithic (~4000 BC), but with substantial genetic contributions from subsequent pan-European cultures such as the Bell Beakers expanding out of Iberia in the Late Neolithic (~2800 BC). Dated haplogroup H genomes allow us to reconstruct the recent evolutionary history of haplogroup H and reveal a mutation rate 45% higher than current estimates for human mitochondria.

GET Conference 2013 live stream

2013 Genomes Environments and Traits Conference Live Webcast
The (sold out!) 2013 Genomes, Environments and Traits (GET) Conference is taking place this Thursday and Friday in Boston. We are celebrating the 60th anniversary of the DNA double helix with an amazing line-up of speakers and Labs.

You may watch the live webcast for free via our new channel at Fora.TV: get2013.fora.tv.

2012 Forbes 400 by ethnic origins

Summary: No dramatic departures from 2009/2010.

1987 (%) 2009 (%) 2010 (%)2012 (%)
Northwestern European 72 51.75 50.551.25
Jewish 23 35.5 35.534.75
Italian 2.25 3.5 4.254.25
East Asian 0.25 2.0 2.02.25
Middle Eastern 1.5 2.25 2.51.75
Greek 0.5 1.5 1.751.5
Eastern European 0.25 1.5 1.751.75
South Asian 0.0 1.25 1.01.5
Hispanic 0.25 0.5 0.50.75
Black 0.0 0.25 0.250.25

Related posts:

Full list below. As always, I welcome any corrections.

The world's richest Jews (an incomplete list)

[Update: see Ethnic origins of Forbes world billionaires (2013) for a more comprehensive list of Jewish billionaires.]

Steve Sailer alerted me to Forbes Israel's list of Jewish billionaires (http://www.forbes.co.il/rating/list.aspx?en6v0tVq=FK), pointing out the number of American Jews appears to be much lower than might be expected based on assessments of the ethnic makeup of the Forbes 400 in 2009 and 2010. As translated by Google:

The world's richest Jews

Jewish billionaires comprise 11% of global billionaires list, and common wealth reaches -812 billion. Who is the top, and in some places deteriorated Mark Zuckerberg?

Having now looked at the 2012 Forbes 400, I see an ethnic breakdown similar to 2009/2010. The Forbes Israel "richest Jews" list was published about a week ago and appears to be put together based on the Forbes World's Billionaires list, which was updated in March 2013. The most recent Forbes 400 was finalized in September 2012, so, while minor differences are possible, for the US the lists should mostly overlap. The Forbes 400 threshold is about $1.1 billion (rather than $1 billion), so we'd tend to expect more US names on the Forbes Israel list than Jews in the Forbes 400 -- if the compilers were thorough. They don't appear to have been.

Intelligence and corruption

Intelligence and bribing behavior in a one-shot game
We investigate the relationship between intelligence and bribing behavior in a simple one-shot game of corruption. We find a robust relationship between intelligence and the probability of bribing in which a higher intelligence quotient (IQ) leads to a lower probability of bribing in the game. This result holds after controlling for other determinants such as gender, attitude toward corruption, and perceptions of corruption. By revealing the gender of the matched player, we also show that gender perceptions of corruption are strong determinants of bribery.
Intelligence and corruption
This study finds that countries with high-IQ populations enjoy less corruption. I propose that this is because intelligent people have longer time horizons.
(Via UDADISI.)

IQ, SES, and criminality

(Via Chuck.) Elaboration on the association between IQ and parental SES with subsequent crime. Personality and Individual Differences 50 (2011) 1233–1237. (pdf)
The current study, based on the nationally representative NLSY data, follows incarceration over a 24-year period. This represents the longest prospective examination of the NLSY crime data to date, since previous analyses have been shorter and is not prospective (Herrnstein & Murray, 1994). With the aim of providing greater confidence in the results, unlike prior analyses the current study uses three major criminological outcomes (onset, incidence and frequency of incarceration), and not one (incidence of incarceration). Based on theoretically reformulated associations between the study variables, the results show that low IQ, low parental SES and their interaction modestly predict the incidence of, frequency of and time to incarceration.

Theoretically, a low IQ may make coping and decision-making difficult and increase the likelihood of crime. Taken in isolation the association between low IQ and increased risk of crime in the current results may be taken as evidence that is consistent with the Bell Curve (Herrnstein & Murray, 1994). Concurrently, however, the present results also indicate that a low parental SES increases the risk of crime, potentially through an inadequate familial environment (Bradley & Corwyn, 2002). These family characteristics may include little emphasis on social attainment. Thus, the current findings indicate that the family environment may provide a route to influence the association between IQ and crime. This possibility is not considered in the Bell Curve view on crime that emphasizes neighborhood SES (Herrnstein & Murray, 1994), and is consistent with opponents to the Bell Curve (Fischer et al., 1996).

Collectively, however, the effects of IQ and parental SES on crime are modestly amplified, as captured by the interaction reflecting unfavorable conditions (i.e., particularly if both IQ and parental SES are low). A possible explanation of this interaction is that a disadvantaged home environment does not encourage social attainment and a low IQ makes coping and decision-making difficult. Taken together this increases the likelihood of crime. Thus these findings support an interactional perspective of crime. Their interpretation is consistent with the usually competing theoretical notions that contrast low SES (Fischer et al., 1996) or low IQ (Herrnstein & Murray, 1994) as factors that increase the likelihood of crime. [. . .]

This study does not separate genetic–environmental influences, unlike past research (e.g., Koenen, Caspi, Moffitt, Rijsdijk, & Taylor, 2006). SES may not purely be an environmental factor that is unrelated to IQ. Parents may give children both genes for IQ and SES (i.e., passive gene–environment associations), and a parent’s SES is partly based on their IQ as a result of life-long active gene–environment interactions. Accordingly, IQ and SES may be moderately correlated due to common genetic influences. Also, as the participants in this study mature, they become increasingly free to create their own environments, partly due to both IQ and SES. The current study, however, affords no assessment of genetics, or upward or downward social mobility, thereby highlighting key directions for future research.

Related posts:

No evidence for higher testosterone in black compared to white adolescent males

Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control. April 2013, Volume 24, Issue 4, pp 817-826

OBJECTIVE: Contrary to the hypothesis that the racial/ethnic disparity in prostate cancer has a hormonal basis, we did not observe a difference in serum testosterone concentration between non-Hispanic black and white men in the Third National Health and Nutrition Examination Survey (NHANES III), although non-Hispanic black men had a higher estradiol level. Unexpectedly, Mexican–American men had the highest testosterone level. Next, we evaluated whether the same patterns are observed during adolescence, the time of prostate maturation.

METHODS: We measured serum testosterone, estradiol, and sex hormone-binding globulin (SHBG) by immunoassay in 134 males aged 12–19 in NHANES III. Mean concentrations were compared by race/ethnicity adjusting for age, Tanner stage, percent body fat, waist, physical activity, tobacco smoke, and the other hormones.

RESULTS: After multivariable adjustment, in the 12–15-year-old males, testosterone concentration was lower in non-Hispanic blacks than whites (p = 0.043), SHBG concentration did not significantly differ between the two groups. Mexican–Americans had the highest testosterone (versus non-Hispanic black: p = 0.002) and lowest SHBG (versus non-Hispanic white: p = 0.010; versus non-Hispanic black: p = 0.047) concentrations. Estradiol concentration was lower in non-Hispanic blacks (p = 0.11) and Mexican–Americans (p = 0.033) compared with non-Hispanic whites. After multivariable adjustment, in the 16–19-year-old males, testosterone, estradiol, and SHBG concentrations did not differ between non-Hispanic blacks and whites. Mexican–Americans had the highest testosterone concentration (versus non-Hispanic white: p = 0.08), but did not differ from the other groups on estradiol and SHBG concentrations. In both age groups, these patterns were generally present, but less pronounced after adjusting for age and Tanner stage only.

CONCLUSION: In adolescent males, non-Hispanic blacks did not have a higher testosterone concentration than non-Hispanic whites, and Mexican–Americans had the highest testosterone concentration, patterns similar to adult males.

This sample is not large, and some of the statistical adjustments may be questionable. But others have also failed to find black-white differences in testosterone among adolescents in unadjusted NHANES data; nor were they seen in a larger study of adolescents,

Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol--the Bogalusa Heart Study.

A large biracial cross-section of 1038 healthy children aged 6-18 yr with 519 blacks, 519 whites, 678 males, and 360 females was evaluated for Tanner stage and serum levels of androstenedione, dehydroepiandrosterone- sulfate, estradiol, progesterone, and testosterone. The anthropometric values of the blacks and whites were very similar at each Tanner stage with only minor differences in age, height, and weight related to an earlier onset of puberty in blacks. The hormones dehydroepiandrosterone- sulfate, progesterone, and testosterone did not exhibit any racial differences. Estradiol showed a significantly higher level among black males compared to white males (P 5 0.05) whereas androstenedione was significantly higher in both white males (P = 0.0001) and females (P I 0.01) compared with blacks.

Alan Templeton's model of human origins

Revolutionizing the “Out of Africa” Story
The human lineage two million years ago was a population with ape-sized brains limited to sub-Saharan Africa. The human lineage expanded into Eurasia around 1.85 million years ago, and our brain size increased throughout the Pleistocene. Anatomically modern humans first appeared in Africa about 200,000 years ago, with anatomically modern forms appearing outside of Africa at more recent dates. [. . .]

One powerful way of extracting this information about past evolution is through multilocus nested clade analysis (MLNCA). This method converts the evolutionary history of a DNA region with little to no recombination into a series of nested branches (clades), which captures time (the deeper the branch in a nested series, the older the time), and then overlays the spatial distribution of the currently observed genetic variation upon the nested series. In this manner, we can estimate the evolutionary history of current variation through both space and time. [. . .]

MLNCA does not require a prespecified model of evolution; rather, the model emerges naturally out of the cross-validated statistically significant inferences. Thus, there is no inherent bias toward any a priori model of human evolution. The cross-validated MLNCA inferences produced a model of human evolution that had some features of previous models, but unique features as well (Figure).

Mass media and public opinion

Radio and the Rise of Nazis in Pre-War Germany
How far can media undermine democratic institutions and how persuasive can it be in assuring public support for dictator policies? We study this question in the context of Germany between 1929 and 1939. Using quasi-random geographical variation in radio availability, we show that radio had a significant negative effect on the Nazi vote share between 1930 and 1933, when political news had an anti-Nazi slant. This negative effect was fully undone in just one month after Nazis got control over the radio in 1933 and initiated heavy radio propaganda.
Steve Sailer: "Gay Marriage" in Ngram: Media Muscle in action
Here's a Google Ngram graph of usage in books of the terms "gay marriage" in red and "homosexual marriage" in blue from 1800 to 2008. The terms were essentially nonexistent until the early 1970s, after which there were a tiny, relatively stable number of references to "homosexual marriage" for two decades. Then there was an inflection point around 1994 and another one around 2003. (Methodology notes: The graph above reflects Ngram's default three-year moving average smoothing. If you turn off smoothing, the inflection points appear a little later than when smoothing is on. Of course, books perhaps lag behind other media because of their longer production cycles.)

I'm fascinated by the mechanics of media muscle reflected in the two inflection points. Here's a topic that had interested almost nobody, straight or gay, for, roughly, ever, yet then in two stages becomes a cultural obsession.

Nate Silver: Gay Marriage Opponents Now in Minority
This is the fourth credible poll in the past eight months to show an outright majority of Americans in favor of gay marriage. That represents quite a lot of progress for supporters of same-sex marriage. Prior to last year, there had been just one survey — a Washington Post poll conducted in April 2009 — to show support for gay marriage as the plurality position, and none had shown it with a majority.

As we noted last August, support for gay marriage seems to have been increasing at an accelerated pace over the past couple of years. Below is an update to the graph from last year’s article, which charts the trend from all available public polls on same-sex marriage going back to 1988.

Miscellaneous links

Audacious Epigone: Skin tone and IQ, and volunteering, too

Human Varieties: Is Psychometric g a Myth?

Jason Malloy: Cryptic Admixture, Mixed-Race Siblings, & Social Outcomes

Bruce Charlton: Harvard is a second rate research university

Staffan's Personality Blog: The Personality of Tribalism (via hbd chick)

Friends Shrink Foes: The Presence of Comrades Decreases the Envisioned Physical Formidability of an Opponent

Face and fortune: Inferences of personality from Managing Partners' faces predict their law firms' financial success

IQ-height correlation partly attributable to pleiotropic genetic factors (not just cross-assortative mating)

The Genetic Correlation between Height and IQ: Shared Genes or Assortative Mating?
In this study, we modeled the covariation between monozygotic and dizygotic twins, their siblings, and their parents (total N = 7,905) to elucidate the nature of the correlation between two potentially sexually selected traits in humans: height and IQ. Unlike previous designs used to investigate the nature of the height–IQ correlation, the present design accounts for the effects of assortative mating and provides much less biased estimates of additive genetic, non-additive genetic, and shared environmental influences. Both traits were highly heritable, although there was greater evidence for non-additive genetic effects in males. After accounting for assortative mating, the correlation between height and IQ was found to be almost entirely genetic in nature. Model fits indicate that both pleiotropy and assortative mating contribute significantly and about equally to this genetic correlation. [. . .]

Taller people tend to be smarter. Although the relationship is modest, height and IQ are consistently correlated at ~.10–.20 [24], [25], [26]. [. . .]

The importance of genetic pleiotropy on the association between IQ and height is notable. On the surface, it might seem that height and IQ involve very different functional systems with different developmental origins. Genetic pleiotropy between IQ and height (indeed, between any two complex fitness traits) is consistent with the idea that variation in these traits partly reflects genome-wide mutational loads, and that these traits are components of attractiveness because of this—i.e., they are honest signals or cues of ‘good genes’ [43], [44], [45]. The additional and substantial increase in additive genetic covariance as a function of assortative mating is consistent with both traits being attractive to the opposite sex.

Related posts:

A model of social class from BBC survey data

A New Model of Social Class? Findings from the BBC’s Great British Class Survey Experiment (pdf):

We analyse the largest survey of social class ever conducted in the UK, the BBC’s 2011 Great British Class Survey, with 161,400 web respondents, as well as a nationally representative sample survey, which includes unusually detailed questions asked on social, cultural and economic capital. Using latent class analysis on these variables, we derive seven classes. We demonstrate the existence of an ‘elite’, whose wealth separates them from an established middle class, as well as a class of technical experts and a class of ‘new affluent’ workers. We also show that at the lower levels of the class structure, alongside an ageing traditional working class, there is a ‘precariat’ characterised by very low levels of capital, and a group of emergent service workers. We think that this new seven class model recognises both social polarisation in British society and class fragmentation in its middle layers, and will attract enormous interest from a wide social scientific community in offering an up-to-date multi-dimensional model of social class.
More:

Obama brain map and the sovietization of science

From Junk DNA to Junk Economics: Beware the Inexorable Sovietization of Big Science

The controversy surrounding the $400-million Encode project’s dubious public relations claims surrounding the function of ‘junk DNA’ and the Battelle Institute’s defense of the $3-billion Human Genome Project (HGP) as economically beneficial (as cited in the recent State of the Union address) make this a good time to examine President Obama’s attempts to bring more of American science under centralized direction and control. [. . .]

The burden of proof for proposed mega-projects should be high, because for every research team working on a billion-dollar, centrally planned National Institutes of Health program, there are hundreds of independent scientists who will go begging. This is a tragedy, as the bulk of our scientific progress—especially in the life sciences—comes not from sclerotic bureaucracies following 10-year plans, but from the genius of independent scientists challenging the status quo.

John Hawks massive open online course announcement

Announcing my MOOC, Human Evolution: Past and Future
Starting in January, 2014, I will be offering a massive open online course titled, "Human Evolution: Past and Future".

This course and all its materials will be open and free for anyone, anywhere in the world. As of this moment, more than 6500 people have already signed up for the course. The course is still more than nine months away, and I'll be developing materials across the entire time up through January. [. . .]

With a worldwide group of thousands of students, we'll be giving people the opportunity to participate in some real research. Some will be as simple as massive measurements of body proportions. Others will be more involved, leading us to...

Looking to the future. The course title is "Human Evolution: Past and Future." To me, the path of our evolution in the past is closely tied to where our species may be going. To that end, the course will be looking at the next hundred, thousand and ten thousand years of our evolution. I'll be interviewing people who are thinking about the impact of technology on our future evolution, and students will come up with their own scenarios based on a strong understanding of the forces that shaped human evolution in the past.

Peopling of Europe book

Jean M.'s book (revised and expanded from her Peopling of Europe website) is now available for pre-order, though it's not scheduled to ship until September or October. I don't necessarily agree with her on every detail, but there's little doubt that on the whole she'll come vastly closer than Sykes, Oppenheimer, or Wells were able to giving an accurate account of the genetic origins of Europeans.

Description and table of contents:

Y haplogroups and aggression in humans

Greg Cochran writes:
If a new environment favored lower (or higher) aggressiveness in males , a Y-chromosome that induced lower (or higher) aggressiveness would take off. And since different Y chromosomes do indeed affect the level of aggressiveness in mice [which I just found out], possibly by affecting testosterone production – this mechanism is plausible. [. . .]

Fortunately for all concerned, the selective value of aggressiveness, etc. has been the same for all human populations forever and ever, before and after the development of agriculture. Otherwise you might see weirdly rapid expansions of particular Y-chromosome haplogroups – common, yet only a few thousand years old.

A 2009 study of 156 Pakistanis found an association opposite what one might expect, but I doubt it would replicate in a larger sample:
Five Y haplogroups that are commonly found in Eurasia and Pakistan comprised 87% (n=136) of the population sample, with one haplogroup, R1a1, constituting 55% of the sampled population. A comparison of the total and four subscale mean scores across the five common Y haplogroups that were present at a frequency > or =3% in this ethnic group revealed no overall significant differences. However, effect-size comparisons allowed us to detect an association of the haplogroups R2 (Cohen's d statistic=.448-.732) and R1a1 (d=.107-.448) with lower self-reported aggression mean scores in this population.
A PhD thesis published this year ("The Y chromosome in cardiovascular disease") looks at reasonably large samples of Polish men and evidently finds no associations between Y haplogroup and sex hormones or aggression:
Though no analysis of the human Y chromosome has ever been completed in the context of these \male-relateda or \sex-specifica phenotypes, evidence from animal models supports a hypothetical role for the Y chromosome in regulation of both aggression and sex hormones. Firstly, the Y chromosome has been repeatedly implicated in aggression in murine models; Gatewood et al. found that female mice carrying an SRY-deleted Y chromosome had significantly higher aggression levels than wild-type female mice, similar to those found in males (Gatewood et al. 2006). Similarly, the Y chromosome was associated with sex steroids through its function in sex determination (Wilhelm et al. 2007).

To identify the mechanism of association between haplogroup I of the Y chromosome and CAD, the effect of this haplogroup on \sex-associateda and \sex-specifica phenotypes was investigated in a series of experiments highlighted in this chapter. No relationship between the Y chromosome and any facet of aggression or sex steroid was identified. These data indicate that these traits are unlikely to drive the association between haplogroup I and increased predisposition to CAD.

(More interestingly, while I haven't looked at the thesis closely it does apparently confirm in Polish men an association between Y haplogroup I and cardiovascular disease, which I hadn't taken too seriously when it was previously reported in British men.)

Although a lack of convincing evidence that major extant European Y haplogroups are differentially associated with aggression doesn't rule out the possibility that Y chromosomes associated with, e.g., lower aggressiveness constituted a larger share of European male lineages in the past, I doubt this possibility as an explanation for the recent expansion of haplogroups like R1b and R1a.

Polynesian mtDNA in C19 Brazilian Amerindians

DNA study links indigenous Brazilians to Polynesians
One broad group of these Palaeoamericans — the Botocudo people, who lived in inland regions of southeastern Brazil — stands out, having skull shapes that were intermediate between those of other Palaeoamericans and a presumed ancestral population in eastern Asia.

Now, a genetic analysis sheds light on the possible heritage of the Botocudo. Pena and his colleagues studied short stretches of mitochondrial DNA (mtDNA) in samples drilled from teeth in 14 Botocudo skulls kept in a museum collection in Rio de Janeiro. By analysing material from inside the teeth, the team minimized the possibility of contamination with DNA from the numerous people who have probably handled the skulls since they arrived at the museum in the late 1800s.

The mtDNA from 12 of the skulls matched a well-known Palaeoamerican haplogroup. But mtDNA from two of the skulls included a haplogroup commonly found in Polynesia, Easter Island and other Pacific island archipelagos, the researchers report today in Proceedings of the National Academy of Sciences1. A separate lab confirmed the result with samples from one of the skulls, indicating that the ‘Polynesian haplogroup’ did not result from contamination, the researchers contend.

The researchers say that it is possible — but unlikely — that the DNA could have come from Polynesians who voyaged from remote islands to the western coast of South America. [. . .]

The researchers also entertain scenarios in which the haplogroup arrived in South America via the slave trade. Around 2,000 Polynesians were brought to Peru in the 1860s, and some could have ended up in Brazil, although the researchers say that they are not aware of any evidence that this occurred. And between 1817 and 1843, approximately 120,000 slaves were shipped from Madagascar to Brazil — and some of them were probably transported to areas where the Botocudo also lived. Although the researchers consider the latter scenario to be the most probable, Pena says: “We currently don’t have enough evidence to definitively reject any of these scenarios.”

“This is a pretty exciting initial result,” says Alice Storey, an archaeologist at the University of New England in Armidale, Australia. Further studies of genetic material from the skulls, including detailed analyses of nuclear DNA (which contains much longer genetic sequences than mtDNA), could offer more insight into the mysterious ancestry of the Botocudo, she says.

The paper: Identification of Polynesian mtDNA haplogroups in remains of Botocudo Amerindians from Brazil

Inbreeding, race replacement, genetic disease, "diversity"

A no more lucid than usual Steve Jones promotes racial mixing in the name of "incest" avoidance in the Telegraph ("Why we’re having less sex with our (genetic) relatives"):

Sir Thomas Beecham – always good for a quotation – once said that “everyone should try everything once, except incest and folk dancing”. Quite where the Morris men come in, I am not certain (although Beecham much disliked the music of Percy Grainger, known for his arrangements of English folk tunes). But when it comes to incest, people are beginning to take his advice. [. . .]

Now it is easy to pick up millions of short doubled-up differences across the whole double helix, rather than in just a few lengthy but untypical segments. A new survey of this kind involved 5,000 random (and supposedly unrelated) Europeans. It revealed hundreds of thousands of previously unknown family links among them, even if one goes back no further than ninth cousins (whose shared ancestor lived at around the time of the French Revolution).

There were, for example, around 30,000 predicted fourth-cousin pairs (a shared great-great-great-grandparent). As a result, taking all family ties into account, the person you sat next to on the bus this morning is, on average, likely to be something like your sixth cousin, which means that the two of you probably share at least one ancestor from the time of the Paris Commune.

Finns (who have a history separate from that of the rest of the continent) and Ashkenazi Jews are even more likely to have close family ties; while in parts of Pakistan, the average relationship of two random people is that of second cousins, with their common ancestor alive at the time of the fall of France.

Sir Thomas Beecham (had he ever met a Pakistani, or even a Welshman) would no doubt have been outraged. But he can begin to cheer up, for in the Western world incest (or at least inbreeding) is on the way out. The proportion of people who identify themselves as of mixed race in Britain has almost doubled in the past couple of decades, and one household in eight contains members of different ethnic origins. For about half of the nation’s children with an Afro-Caribbean parent, the other parent is white, so that on these islands the pedigrees of two continents will soon merge.

Two dictionary definitions of "incest":

sexual intercourse between two persons commonly regarded as too closely related to marry

the crime of sexual intercourse, cohabitation, or marriage between persons within the degrees of consanguinity or affinity wherein marriage is legally forbidden.

Possibly Steve Jones (a Welshman married to a Jewess) would like to see intraethnic marriages among the English outlawed. But I can be fairly certain most English feel otherwise, and it takes extreme vileness to conflate normality (intraethnic mating) and incest.

Yes, as basic math would inform us, some degree of inbreeding will exist in any population of finite size. No, the level of inbreeding present in the British population does not represent a cause for concern (and even if it did, it would not be solved in the long run by mulattoizing Britain). Empirically, mild inbreeding (yet more extreme than seen in the typical intra-English marriage today) appears to be associated with greater fitness in Europeans:

Our results, drawn from all known couples of the Icelandic population born between 1800 and 1965, show a significant positive association between kinship and fertility, with the greatest reproductive success observed for couples related at the level of third and fourth cousins.
As for deleterious recessives, outbreeding may temporarily mask harmful alleles but provides no help in the long run. Neel:
A second obvious genetic departure of most of the civilized world from tribal societies is the relaxation of inbreeding. A discussion of the consequences of such relaxation rapidly becomes complex, and we will consider only the simplest case, involving diseases due to completely recessive genes with quite deleterious effects, incompatible with reproduction. [. . .] When inbreeding is relaxed, as is now particularly the case for Christian communities, homozygosity for genes of this type decreases, and there should be a decrease in the diseases associated with these genes. This, however, is only temporary. Mutation pressure continues, and the gene frequency will very slowly build up, until finally the frequency of homozygotes will again come into balance with mutation pressure. However, the relative frequency of the heterozygotes in the population is now greater than before. Should this population ever revert to high levels of inbreeding, it would, so to speak, "pay the bill," i.e., the gene frequency would have risen above the frequency consistent with the new level of inbreeding, and there would now temporarily be more of whatever disease is associated with the genes in question than would be the case had inbreeding continued at the original levels. Furthermore, there is evidence from experimental genetics that the heterozygotes for these recessive genes are sometimes themselves slightly disadvantaged, so that a relative increase in the frequency of the heterozygous carriers of a deleterious recessive gene is not to the advantage of the population.
One might almost be driven to question the sincerity of Jones' concern with the genetic welfare of the British. Prospective parents can already check their carrier statuses (and/or screen embryos) for most "common" Mendelian diseases, and this sort of thing will only become cheaper and more broadly applicable in the future.

Also note that basic math doesn't cease to be true just because you mongrelize a population. Turn Britain mulatto, and (besides the fact that, again by basic math, humans as a species are obviously "inbred" -- just like every other species) only the first generation will be maximally outbred. Mate two mulattoes, and you can expect them to have both segments European or both segments African across much of their genome, meaning any benefits of heterosis received by F1 mulattoes (and none to my knowledge have ever actually been demonstrated) will be greatly reduced in the next generation. Inbreeding will also commence building up in the new mulatto population just as it would in any other population with similar a demographic profile, with lineages being lost over time.

Or possibly Jones would like to maintain high levels of immigration from Africa, which ultimately would have the effect of simply replacing the English with Africans. That again would fail to solve the (non-)problem of inbreeding -- though it would certainly solve the English problem, which would appear to be the important thing to people who share Jones' politics.

Make the entire world panmictic, and you still do not "solve" inbreeding. Basic math continues to apply. Lineages will still be lost. It's just that now when a lineage is lost, it will be lost from the entire human population. As it happens:

V.13 Avoiding Inbreeding.

Interestingly enough, the systems of “maximum avoidance of inbreeding” do not have the lowest ultimate rates of approach to homozygosity. With the same number of individuals, it is possible to devise circular half-sib mating systems which, although they inbreed faster initially, have a lower rate of approach to total homozygosity. This was shown by Kimura and Crow (1964), who treated such systems in generality. Robertson (1964) provided a more general framework for this result. He showed that, in general, regular systems of mating with a given number of individuals will have a lower rate of approach to homozygosity the more closely related are the individuals who mate!

Of course, the best system of all for avoiding the loss of alleles from a population of fixed size involves the most intense inbreeding of all. If we divide a population of size 20 into 10 full-sib lines, and keep those lines isolated from each other, we stand a good chance of retaining a reasonable fraction of the common alleles present initially. For even though each such line reaches fixation for an allele, different lines may well fix for different alleles. So although each individual becomes homozygous, we can restore a good fraction of the initial heterozygosity of the base population by crossing different lines. By contrast, a repeated mating system which does not break the population into isolated lineages is certain to fix for one allele or another sooner or later, however small its rate of approach to homozygosity.

[Joe Felsenstein. Theoretical Evolutionary Genetics.]