Genetic Interests vs. Inclusive Fitness

A distinction.

In On Genetic Interests, Salter makes a careful distinction between genetic interests and inclusive fitness:

Genetic interest is not inclusive fitness…

Genetic interests are:

…the numbers of copies of an individual’s distinctive genes.

I would rephrase that a bit to “distinctive genetic information” so as to include genetic structure, genetic integration, etc. – higher levels of genetic information as opposed to the “beanbag” genetics counting of gene copies. In contrast, inclusive fitness is:

 …the effect of an individual’s behavior on the reproduction of his distinctive genes in himself and others (usually kin and fellow ethnics).

Genetic interests are innate while inclusive fitness depends upon behavior and choices made.  A person always has a certain amount of genetic interests but if they act to promote those interests than their inclusive fitness is positive, if they do nothing their inclusive fitness is zero, and if they act against their genetic interests then their inclusive fitness would be negative.

Salter gives examples of this in his book; I’m not going to repeat that here. You should have the book and look it up yourself. What I want to do here is link these concepts to my idea of gross vs. net genetic interests.

The “raw” genetic interests, as defined by Salter, are in a sense the “gross genetic interests” but the actual final outcome of genetic interests, the net genetic interests, is influenced by inclusive fitness and any other factors affecting genetic interests. Thus:

Net genetic interests = gross genetic interests +/- inclusive fitness possibilities and other factors affecting genetic interests.

Net genetic interests are the end result of what the genetic interests are when all factors are considered that influence the gain or loss of genetic interests. Gross genetic interests would be the innate, theoretically (but not practically) maximally possible, optimal level of genetic interests, independent of real world influences and independent of costs/benefit considerations leading to decisions on how to actualize inclusive fitness in pursuit of genetic interests.  

A lack of understanding of gross vs. net genetic interests can lead to problems. This can take place even within a narrow ethny.  An English nationalist may become obsessed with the very minor genetic differences between East and West England and/or North and South England and believe that full maximization of ethnic genetic interests would be to separate England and the English people along those lines and to focus only on that area most aligned to your genetics. One can easily see how this attempt to maximize gross genetic interests by pursuing tiny diminishing returns of genetic distinctiveness can be damaging at the level of net genetic interests. Such an absurd pursuit of genetic interests would divide the English people against themselves, destroying the organic solidarity of the nation, weakening them, and making them all more vulnerable to outsiders who are more genetically divergent. In this case, the narrow pursuit of optimal gross genetic interests would constitute a negative inclusive fitness, decreasing net genetic interests, while taking a more practical approach in supporting the entire English ethny would be a positive inclusive fitness, leading to increased net genetic interests. When genetic distinctiveness is very small and especially in the context of competition with more genetically divergent others, one maximizes the net payoff of genetic interests by ignoring tiny differences and realizing that, in contrast to more alien peoples, you have significant genetic interests in closely related groups, and cooperation with such closely related groups can also enhance the well-being of even your most narrow group.

Likewise, in a global context, petty nationalist ethnonationalism may seem a way to maximize ethnic genetic interests by investing all of your higher-level (e.g., ethny-level) inclusive fitness efforts only on your specific ethnic group. But if the well-being of that group is, in the long term, best served by inclusion in a race-based nationalism (e.g. pan-European White nationalism), then the narrow focus on ethnonationalism could actually be detrimental to ethnic genetic interests and reflective of a negative inclusive fitness. Add to that the reality that distinctive genetic information exists on the racial, as well as the ethnic, level, then focusing on ethnonationalism excludes the genetic interests at a higher group level and is again reflective of negative inclusive fitness. We can then add to the equation the possibility of kinship overlap between members of closely related ethnies belonging to the same race and once again a strict petty nationalist focus can be maladaptive. In these cases, net genetic interests are best served by adding racial nationalism to ethnic nationalism, while the gross genetic interests would be the theoretical maximization of genetic interests by focusing on a narrower unit (putting aside the problem of kinship overlap and of deciding what narrower unit is actually the one you should genetically identify with). The overall factors favor inclusive fitness serving net genetic interests; such inclusive fitness is positive while those that do not serve net genetic interests are zero or are negative. Thus, positive inclusive fitness serving net genetic interests for Whites is represented by pan-Europeanism, while zero or negative inclusive fitness is represented by petty nationalist ethnonationalism.

Fst vs. Genetic Kinship

A comparison.

I would like to provide a crude, very simplified, but useful, explanation of Fst vs direct measures of genetic kinship, and again state my preference for the latter.

Let us start with Fst, which is a measure of how to divide genetic variation within or between groups. Consider two populations A and B (these each can also be considered subpopulations of the entire A+B total population).  We can consider the total genetic variation of A+B, at whatever alleles evaluated, and then ask how much of that is due to genetic variation within each (sub)population and how much is due to genetic differences between these (sub)populations.  Thus, the total genetic variation can be apportioned to the within vs. between components, and the between component is the Fst.  It stands to reason that if A and B are genetically similar then the between fraction will be small and hence Fst low, since very little of the total genetic variation of A+B is due to A vs.B. On the other hand, if A and B are more genetically distant then a greater proportion of the total genetic variation is explained by the differences of A vs. B and hence Fst will be higher. We can see that Fst is therefore a direct measure of relative genetic variation but an indirect measure of genetic differentiation and distance.

Genetic kinship asks something somewhat different. Here we are determining how many of the gene sequences of A and B, at whatever alleles evaluated, are the same and how many are different.  This is a direct measure of genetic similarity (and differentiation/distance) – thus a direct measure of genetic kinship between the genomes studied. The genetic kinship can be measured relative to some background level and/or to various other groups, and one could then ascertain relative levels of genetic kinship, whether it is greater than background (a positive value) or less (a negative value).  One could also rank groups, and compare individuals to groups (or to each other), and measure genetic kinship for all of these comparisons.  It is genetic kinship that is directly related to ethnic genetic interests and thus genetic kinship is biopolitically relevant.

Harpending demonstrated the relationship between Fst and genetic kinship and how the former could be used to get some sort of measure of the latter.  However, just measuring genetic kinship directly is best, without needing to go through the Fst intermediary and dealing with issues affecting the Fst measures, such as the dependence of Fst on subpopulation (e.g., A vs. B) heterozygosity (and of course which (sub) populations are chosen for the comparison).

Further, the relationship, such as it is, between Fst and genetic kinship is likely only relevant at the lowest level of genetic integration, at the level of allele by allele “beanbag genetics” analysis (considering elementary genic differences).  If one looks at higher levels of genetic integration, the relationship may break down. It is always best to just look directly at genetic kinship – how similar are gene sequences (lowest level of genetic integration) or how similar are genetic structures (e.g., correlations of genetic sequences) (higher levels of genetic integration).  

Direct measures of genetic kinship tell us what we really want to know – how similar or different we are to others, genetically speaking, who is more or less our genetic kin.  Yes, you can do a “work around” with Fst or other measures, but why should we need to do that, with all of the possible problems and limitations that may ensue?  Just measure genetic kinship.

Genetic Integration Redux

Let us consider together.

Blog category.

See this.

Final Conclusions

1. Although the analysis has limitations, it demonstrates that human genetic differentiation increases as genetic structure is considered.

2. A considerable amount of this increase in genetic differentiation is at the single-locus level, which I had not previously considered as being that important.

3. Most importantly, the multiple-locus analysis shows complete differentiation.

4. A problem in this analysis is with the scalability of the multiple-locus determinations, and the program is unable to evaluate the entire genetic structure concept; better methods, analyzed with better data, are required.  In the meantime, it would be useful to even just have more in-depth analyses using DifferInt.

5. When all is said and done, this analysis, even with its limitations, extends the EGI concept.

References

1. https://www.uni-goettingen.de/en/124871.html

2. Gillet, E.M., Gregorius, H.-R. (2008) Measuring differentiation among populations at different levels of genetic integration. BMC Genetics 9, 60. http://dx.doi.org/10.1186/1471-2156-9-60

3. Gillet, E.M. (2013) DifferInt: Compositional differentiation among populations at three levels of genetic integration. Molecular Ecology Resources 13, 953-964. http://dx.doi.org/10. 1111/1755-0998.12145

See this.

It might be a good idea to review my idea of genetic structure again here.

Genetic structure as per my definition can be viewed as a form of linkage disequilibrium of alleles over all the loci in the genome, or this distinctive genome, of at least whatever number of loci that were assayed.  Each specific permutation of multilocus genotypes is a discrete entity, so that one would expect, of course, district genetic structures between any set of individuals who are not identical twins; there would be differences in genetic structure within families, never mind within ethnies.

However – and this is the key point that separates my idea from the run-of-the mill evaluations of genetic structure – I envision genetic structure to be defined by specific ranges of multilocus genotypes.  Therefore, while there is going to be, naturally, individual variation of discrete multilocus genotypes within families, there will be a family-specific range of multilocus genotypes, a range within which all the individual genotypes, of that family will fall within.  Likewise, there will be ethny-specific ranges of multilocus genotypes, so that members of an ethny will exhibit genotypes that – while they differ on an individual level – will fall within a range, a set, of genotypes characteristic of that ethny.  

It then follows, that while multilocus genotypes will be differentiated from each other, the extent of that differentiation will differ.  Different families will exhibit different ranges, or sets, of possible multilocus genotypes, but families belonging to the same ethny will exhibit ranges that are more similar to each other than that of families of different ethnies (the same goes for individuals of course, across families or across ethnies).  Ethnies belonging to the same continental population group (i.e., intra-racial) will exhibit more similar ranges of possibilities of multilocus genotypes than that of inter-racial comparisons.  One could think of it also as frequency distributions of multilocus genotypes, of all the alleles possibilities at all the relevant loci considered together as a discrete entity, and one can compare how similar the frequency distributions are, with more overlap from those more similar.  

One would also expect a solid correlation, or association, between the differentiation as measured by an allele-by-allele genepool/beanbag approach, single locus genotypes, and multilocus genotypes. The relative extent of differences should correlate in at least a qualitative sense between these levels of “genetic integration.”  Hence, as previously noted at this blog, “complete differentiation” at the multilocus genotype level should differ in extent dependent upon how similar or different the genotypes are from each other.  One should in theory be able to quantitate this in a continuous fashion, rather than just having a binary yes/no undifferentiated/completely differentiated choice.

This is obviously an important topic.  If we are to make decisions based on genetic interests, don’t we need to have a better understanding about what those interests actually are, quantitatively speaking?

If we look at the original Gillet and Gregorius paper, even when including the continuous measures of elementary genic differences, instead of the disjunctive measures of neglecting elementary genic differences, the oak stand genetic data show a ~ 50% increase in differentiation going from gene pool to single locus and an ~ three-fold increase form gene pool to multiple locus.  If these findings are comparable to the human situation, then even when considering the non-disjunctive multiple locus comparisons, genetic differentiation between human groups is likely to be several fold higher than previously calculated with the “beanbag” genepool methods, such as that used by Salter in On Genetic Interests.  Hence, ethnic genetic interests are even greater, when considering genetic structure and genetic integration, than previously thought, and the harm caused by diminution of these interests, consequently greater.  Further, the idea of “more hybrid children can compensate for the loss of genetic interests because of inter-breeding” is shown to be much more fraught with problems and difficulty.  If we then consider the more disjunctive measurement of genetic integration of neglecting elementary genic differences, then the harm cause by the diminution of ethnic genetic interests becomes enormously greater, and, importantly, no number of hybrid children could compensate for racial miscegenation – multilocus differentiation approaches, or equals, 1.0, and thus the original genetic structure cannot be compensated for by merely increasing copies of genepool (or even single locus) genetic information.

It says a lot – and all negative – that no population geneticist has attempted to apply the DifferInt program to human genetic data. Political considerations from the Left would dissuade the production of data that would show that human genetic differentiation is much greater than previously though. Such data would absolutely revolutionize the concept of ethnic genetic interests (Salter needs to revise his work to incorporate these concepts).  We need someone – if even “amateurs” – who have the computational resources, expertise, access to human genetic data, and the time, to generate these data. Unfortunately, I currently am not in a position to do so (or else I would have done so), apart from the small scale work linked to above. This needs to be done.

Brief Harpending Notes

In all cases, emphasis added.

You should read the entire paper, which was reproduced in the Appendix of Salter’s On Genetic Interests; Harpending’s work in this regard was an important foundation for the genetic section of Salter’s work. Here I will very briefly comment on a few excerpts from Harpending’s paper.

Abstract:

The coefficient of kinship between two diploid organisms describes their overall genetic similarity to each other relative to some base population. For example, kin-ship between parent and offspring of 1/4 describes gene sharing in excess of random sharing in a random mating population. In a subdivided population the statistic Fst describes gene sharing within subdivisions in the same way. Since Fst among human populations on a world scale is reliably 10 to 15%, kinship between two individuals of the same human population is equivalent to kinship between grandparent and grandchild or between half siblings. The widespread assertion that this is small and insignificant should be reexamined.

Fst is a flawed metric and we need direct assays of kinship, but, that aside, let us concentrate on the last two sentences there. Against the background of humanity, co-ethnics have kinship equivalent to that “between grandparent and grandchild or between half siblings.” Harpending’s comment that “[the] widespread assertion that this is small and insignificant should be reexamined” is therefore a considerable understatement. Consider also that neither Harpending nor Salter dealt with issues related to genetic structure/genetic integration, which would make group differences even more marked. Genetic group differences, and the ingroup kinship consequent to those genetic differences are not only highly significant, I would argue that for humans there is nothing more significant. This constitutes our ultimate interests as evolved organisms.

When Hamilton and others described the theory they often spoke in terms of gene identity by descent, thinking for example of the one half of the nuclear genes the in a diploid offspring that are identical to those in the parent. Many authors also spoke of shared genes. Neither of these descriptions is completely accurate. I may share many genes with, say, an onion…

I’ve stressed this point many times, including and especially when debating mendacious HBDers and their attempts to delegitimize the concept of ethnic genetic interests. The issue is not mere gene copies; it is not true that a White has more interests in two or three Negroes than in two Whites given the possibility of greater number of their gene copies present in the former than the latter.  A person does not have more genetic interests in an onion crop than in another human. It is the distinctive genetic information that is important, the gene sharing above and beyond random sharing, the relative genetic kinship. And that’s not even considering higher order genetic structure.

Kinship coefficients in a random mating diploid population are simple and well known. For example, pick a gene from me, then pick another gene from the same locus from me. With probability 1/2 we picked the same gene, while with probability 1/2 we picked the other gene at that locus. Therefore the probability that the second gene is the same as the first is just 1/2 + p/2, and substitution of this conditional frequency in the formula for kinship shows that my kinship with myself is just 1/2. 

This is crucially important, and helps put Lewontin’s mendacity in the proper perspective. In theory Fst can range from 0 to1; in practice it is very rare, in any organism, to observe values greater than 0.5. Consider Harpending’s proof of the relationship between kinship and Fst (note: relationship, not identity; direct kinship assays would be superior to measures of relative genetic variation such as Fst). If an individual human has kinship with themselves at only 0.5, and if Fst (a measure of relative genetic variation) is correlated with kinship, then of course you are always going to observe “more genetic variation within than between” human groups – essentially half of that variation can be considered inherent in single individuals.

The same reasoning leads to the well known values of 1/4 with my child, 1/8 with my grandchild, my half-sib, or my nephew, and so on. It is very important that the coefficient of kinship not be confused with the coefficient of relationship. These are conceptually and numerically different creatures. The coefficient of relationship can be thought of as “fraction of shared genes” between two organisms

See this. As Harpending notes, in a random breeding population, the coefficient of relationship is twice that of kinship (or kinship is half that of relationship); however, that can be altered with inbreeding, population structure, etc.

Many studies agree that FST in world samples of human populations is between ten and fifteen percent. If small long-isolated populations are included, the figure is usually somewhat higher. A conservative general figure for our species is FST 0.125 = 1/8. This number was given by Cavalli-Sforza in 1966, and a widely cited paper by Lewontin (1972) argued at length that this is a small number implying that human population differences are trivial. An alternative perspective is that kinship between grand-parent and grandchild, equivalent to kinship within human populations, is not so trivial. For further discussion see Klein and Takahata (2002, pp.387–390).

See what I wrote above. Thus  “…not so trivial” is a monumental understatement.  What could be more important?