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for your consideration, a review by andrew sabisky of tatu vanhanen‘s Ethnic Conflicts: Their Biological Roots in Ethnic Nepotism (links added by me). thanks, andrew! (^_^)

Ethnic Conflicts: Their Biological Roots in Ethnic Nepotism – some thoughts

Nationalism, once thought to be a monster whose thirst for blood had been thoroughly slaked by mass warfare, is making a resurgent comeback throughout Europe. Ostensibly fired by opposition to both Islam and the European Union, Marine le Pen & Geert Wilders – amongst others – have made major polling gains: future electoral victories promise or threaten, depending on your point of view. Golden Dawn have already achieved ballot box success in Greece. Robert Putnam’s work shows that interindividual trust in America has undergone a spectacular decline since the 1960s, accompanying the rise of ethnic diversity. In fact, recent modeling by unwilling sociologists shows that not even in 20 million possible worlds can ethnic diversity increase without a consequent decrease in community harmony. But why?

Tatu Vanhanen, perhaps best known in the Anglosphere for his co-authorship (with Richard Lynn) of such blockbusters as IQ and Global Inequality and IQ and the Wealth of Nations, has some answers. Vanhanen, inspired by the work of renowned scholars such as Pierre van den Berghe and J. Philippe Rushton, traces the roots of ethnic conflict to the sociobiological theories of inclusive fitness and genetic similarity. Despite vast variation within ethnic groups, members of ethnic groups will, on average, be more closely related to each other than random members of other ethnic groups, making ethnic nepotism an evolutionarily adaptive strategy. Ethnic nepotism is family nepotism writ large; the same process is driven by selfish genes aiding the replication of identical genes resident in related others. Ethnic groups are super-families, though the degree of difference between families varies. Races separated by geography for millennia differ more greatly than more recent cleavages within the Indo-European language-family (for example).

So far, so mainstream – at least in sociobiological terms anyway. The most intriguing aspect of Vanhanen’s introduction was his definition of ethnic conflict. I had been expecting ethnic conflict to be operationalized purely in terms of violence, an expectation aided by the macabre pile of skulls on the front cover. But Vanhanen includes peaceful conflict as well: his model incorporates all forms of intra-nation ethnic division, whether they take the form of political parties politely debating in parliaments, or destructive mobs engaged in ethnic cleansing. His scale has 5 levels: at level 2, for example, political parties or major interest groups are routinely organized along ethnic lines, and some level of discrimination is present. At level 4 discrimination and repression are high and systematic, and there is some serious level of civil warfare or terrorism.

Anyway, after compiling and computing data for 176 nations, Vanhanen reveals that the level of ethnic heterogeneity explains 66% of the variance in the level of ethnic conflicts, the remainder to be explained by other factors and measurement error. The expected relationships between democratization and national income levels and ethnic conflicts exist, but are weak. Intriguingly, he notes that while democratization does not reduce ethnic conflict much, it does tend to reduce violence somewhat; the countries with high levels of ethnic heterogeneity but lower-than-expected levels of strife tend to be either democracies of decent quality or strong autocracies. The two successful recipes for restricting ethnic violence seem to be either democratic institutions specifically adapted to the demands of blood, or the brutality of a hegemonic dictatorship, though obviously the sample sizes for countries with large residuals are not particularly great. Vanhanen also notes that high levels of interracial marriage seem to lead to more stable situations than one might expect, though such a strategy perhaps comes with other costs.

This is just a very brief sketch of Vanhanen’s work, which is well worth exploring in more depth. His nation-by-nation account of the factors that perhaps account for each country’s position on the regression line is fascinating and not something I can do justice to here (so please do buy your copies from Richard Lynn’s Ulster Institute).

As mass immigration irrevocably changes the face of the West, when will it also change our political cultures? Can they adapt to the new and unexpected requirements of sociobiological logic? The implications are intriguing to trace. In the face of declining trust and divergent genetic impulses, can the British constitution – which has until now defied codification – survive? Perhaps the rules of the game will need to be written down in one place in the future – until now we have rather muddled by on trust and precedent. Will institutionalized power-sharing (as in Northern Ireland) become the norm in the West – not between Catholic and Protestant, but between Muslim and non-Muslim (by around 2050 Britain is forecast to be a majority Islamic nation on current birthrate trends)? How much internal resistance will there be to the adaptation of current institutions? How much of the resistance, and counter-resistance, will be violent?

These questions are currently not a significant part of political debate, but Vanhanen’s incisive and clearly written work suggests that perhaps they should. I confidently recommend it in the expectation that many potential readers will derive their own interesting and worthwhile hypotheses from his data and analyses.

*update 10/27: for more on human leukocyte antigens (hla’s), see chris davies’ blog right here! (^_^)
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over the past few months, commenter chris davies has left several interesting comments here on the blog about hla haplotypes (see here and here and here and here for example) — something about which, like so very many things, i know absolutely NOTHING.

i asked chris if he’d help alleviate my ignorance by writing a post on the topic, and he has graciously obliged (thanks, chris!). so, without further ado, here’s chris’ introduction to hla!:

An Introduction to HLA (Human Leukocyte Antigens)

I would like to thank HBD Chick, who recently asked me if I wanted to write a guest post here about Human Leukocyte Antigens (HLA). I have been a reader of this blog for several months now, and I really enjoy it. This blog is among the most innovative of the HBD-related blogs out there and takes a completely different approach to the subject. So it is a pleasure to write a post here, as I don’t write a blog myself.

In the comments section on some posts here recently I have talked about ‘HLA haplotypes’. I have had an interest in HLA haplotypes for a few years, following discussions with a molecular biologist who writes (or rather wrote) in newsgroups including Usenet. But what are ‘HLA haplotypes’, and more importantly what is their usefulness or relevance to those of us with an interest in ‘HBD’?

‘HLA’ means Human Leukocyte Antigen. The HLA system is simply the name given to the human version of the Major Histocompatibility Complex (MHC). MHC genes are found in most vertebrates, and this group of genes can be found on chromosome 6.

HLA genes are important in immune function and disease defence. There are three classes: Class I (A,B,C); Class II (DP, DM, DOA, DOB, DQ, DR); and Class III. All play different roles.

In addition to conferring resistance or susceptibility to various diseases and conditions (eg autoimmune diseases, such as type I diabetes), they are also vitally important in organ and bone marrow transplants. For example, if a donor is not a close enough match in terms of HLA, an organ could be rejected. Because diversity of HLAs in human populations is a part of disease resistance, it is very uncommon to find two unrelated individuals with identical HLA molecules at all loci.

In addition, it has been claimed that HLA may play a role in human mate selection through people’s perception of the odor of other people.

HLA haplotypes are like strings of HLA genes by chromosome, with one being inherited maternally and the other paternally. A multigene haplotype is a set of inherited alleles covering several genes, or gene-alleles. Common multigene haplotypes are generally the result of identity by descent from a common ancestor. As distance from the ancestor increases, chromosomal recombination causes multigene haplotypes to fragment.

An example of an HLA haplotype is shown below:

A*01:01 ; C*07:01 ; B*08:01 ; DRB1*03:01 ; DQA1*05:01 ; DQB1*02:01
[Which by serotyping, is more simply: A1-Cw7-B8-DR3-DQ2].

This particular haplotype btw is found at high frequency among people of North-West European descent, including Irish, British, Dutch, Germans, Scandinavians, and of course a high percentage of Americans and Australians. It is associated with autoimmune disorders like coeliac disease, and allergic diseases like hayfever and asthma.

In addition to medical use, HLA haplotypes can also be used as a means of tracing migrations in the human population as they are like a fingerprint of an event that has occurred in evolution.

So alongside Y Chromosome DNA and Mitochondrial DNA (mtDNA) markers, HLA haplotypes are useful tools for molecular anthropologists in determining evolutionary links between ancient and modern human populations. They also help to determine closeness of relationships between or within populations, and commonality of geographical origin between groups. Therefore patterns of migration and settlement can be traced, giving insight into how contemporary populations have formed and progressed over time.

Because the HLA system is under selection, diversity in HLA should be looked at in conjunction with other markers like Y-DNA and mtDNA in building a bigger picture when tracing migrations of modern humans.

However, HLA has several advantages over Y-DNA and mtDNA. mtDNA is often biased towards the founders in a core population and can show a punctuated distribution, while Y-DNA is biased more towards relatively recent migrations, and with both of these markers the effects of genetic drift are more rapid. With HLA there is intense heterozygous selection which works to preserve diversity.

Also with HLA, one tends not to see a punctuated distribution of haplotypes across geographical regions between groups, but rather one sees a fluidity of migrations tracing back to their original source population. Examples of this occur when one looks at diversity of HLA in northern Africa, which appears to be the source for a number of haplotypes that migrated into Europe in the Holocene. This picture is less clear from looking at mtDNA or Y-DNA data only.

Finally, the other advantage of HLA is the sheer volume of data available. [See: www.allelefrequencies.net]. The numbers of people worldwide who have been typed for HLA are huge. There are nearly 22 million donors and blood cord units in the BMDW (Bone Marrow Donors Worldwide) database, encompassing many different ethnicities and nationalities with hundreds of thousands of HLA alleles and extended haplotypes identified. Y-DNA and mtDNA cannot offer this volume of data. Whether used for tracing ancient human migrations, or researching diseases in different populations, this data can be extremely helpful.

The association of HLA haplotypes in populations with certain diseases in Western countries is interesting to consider from an HBD perspective. For example, if resistance or susceptibility to obesity, heart disease, diabetes, breast cancer, etc. are all affected by HLA type, then there could be wildly varying outcomes between different population groups, in addition to the effects of environmental or lifestyle factors.

This in turn could have serious implications. For example, certain disease-related charities’ fund-raising campaigns are aimed at convincing the general public to donate cash on the basis that everyone is almost equally at risk from that particular disease, when different ethnic groups living in the same country with the same lifestyle may often vary in risk considerably from very high risk down to very low risk, with HLA type being an important determining factor. But the charity may not publicise this information in order not to jeopardise their fund-raising. This, I should stress, is speculation on my part however.

If want to find out more about Human Leukocyte Antigens, please refer to some of the sources listed below:

References
– The Allele Frequency Net Database (AFND). A database and online repository for immune gene frequencies in worldwide populations: [www.allelefrequencies.net]
“Tracking Human Migrations by the Analysis of the Distribution of HLA Alleles, Lineages and Haplotypes in Closed and Open Populations.” [Fernandez Vina, M. et al, 2012].
“HLA 1991: Proceedings of the Eleventh International Histocompatibility Workshop and Conference” (Volumes I & II) [Kimoshi Tsuji; Miki Aizawa; Takehiko Sasazuki] Oxford Science Publications, 1991.
– “HLA-Net: A European Network of the HLA Diversity for Histocompatibility, Clinical Transplantation, Epidemiological and Population Genetics.” [www.hla-net.eu].
– “AHPD: Analysis of HLA Population Data to Reconstruct the History of Modern Humans and Infer the Role of Natural Selection.” [geneva.unige.ch/ahpd].
“Challenging Views on the Peopling of East Asia: the Story According to HLA Markers.” [Di D, Sanchez-Mazas A.]. Am J Phys Anthropol. 2011 May; 145(1):81-96.doi:10.1002/ajpa.21470.Epub2011Jan4. PMID:21484761 [Pubmed – indexed for MEDLINE].
– Wikipedia: “Human Leukocyte Antigen.”
– Wikipedia: “Major Histocompatibility Complex.”

(note: comments do not require an email. gene map of the human leukocyte antigen (hla) region!)

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