I may have to make “misdreavus” a co-blogger here at some point, considering how I quote him here. But, in defending HBD (Human BioDiversity), he has made a nice basic summary of the reasons why we believe in HBD (that is, overwhelming evidence).
This was all in response to social anthropology scholar A. J. West, who some of you may remember from Cochran’s & Harpending’s. West wrote a post critical of HBD. I’m not going to recite anything from it, because it is a long drawn-out collection of strawman arguments and nonsense. But misdreavus’s response to West was an impressive review of the case for HBD. I am going to annotate it with links to references to his claims (emphasis in original):
1) The scientific basis behind so-called “human biodiversity” (or HBD) is blessedly simple in its obviousness, albeit one that goes shockingly under-acknowledged by most who call themselves authorities in the human sciences. We already have enough evidence that genetic variation in the human species must account, in some non-trivial way, for the variation in phenotypic diversity we see among the major extant human populations living today. By that I refer not only to salient differences such as the height gap between Aka Pygmies and Congolese Bantus, or that fact that west Africans have more prognathous jaws than northern Europeans, but also artifacts of our biochemistry such as Type II diabetes (which usually correlates with obesity) or alcohol metabolism (a large percentage of east Asians have abtabuse built into their genomes — Greenland Inuits don’t). Of course. We get it. There is inter-ethnic (or inter-demic, or inter-population — feel free to choose whatever taxonomic subdivision du jour is fashionable these days among the PC crowd) variation for virtually every single trait for which there exists variation among members of a single ethnic group: no two Irishmen have noses that are exactly the same shape, and neither do any two races, on average. No two Koreans have skin color that is exactly the same hue, and there is a vast gap in skin color between Norwegians and Dinka. No two Russians are of exactly the same height — not even identical twins, and virtually every single Swede is taller than every single Mbuti pygmy. This much is obvious to anyone with an unimpaired frontal lobe.
And we can extend this reasoning not only to the aforementioned physical traits (and much more), but also cognitive skills, however they are defined in every single culture — for virtually every single behavioral trait ever documented among human beings is heritable. [see All Human Behavioral Traits are Heritable] We know that two children who are reared by the same pair of parents can be strikingly different in their behavior and temperament, and that these differences almost always persist long past childhood. It matters not how “personality’ and “temperament” are defined, or that there are not, never have been, and likely never will be any precise definitions of these terms that are useful to psychological science. (Let us avail ourselves of the postmodernist obscurantism, trenchant reality denial, and casual know-nothingness that you decried earlier in a post about social anthropology. It is enough for us to acknowledge that no two humans are alike in behavior, and that the human mind is not a blank slate.) Behavioral differences between any two people, even identical twins, manifest themselves starting from birth, and they only magnify throughout the lifespan. Not surprisingly, it has been demonstrated that babies from different ethnic groups also demonstrate behavioral differences from the cradle. East Asian babies, on average, tend to remain placid and calm when a soft cloth is dropped over their faces — west African and European babies are the polar opposite. See here: http://westhunt.wordpress.com/2013/03/16/dan-freedmans-babies/ [see also this video]
If, indeed, it is the case that human beings vary in behavior, and if it has been proven that much of this variation in behavior may be attributed to hereditary causes, then this alone is sufficient to demonstrate that heredity must explain some of the variation in cognition between any two human populations who vary in their evolutionary history. Well, has this been proven? Of course it has. [see How Much Hard Evidence Do You Need?]. “Heritability”, as the term is implemented in quantitative genetics, refers to the portion of variation in a phenotype within a population that may be attributed to heritable differences, given a certain range of genotypes and phenotypes: H^2 = Var(G)/Var(P). The classical twin study, as much as it is ballyhooed by idiots in the social sciences who are reality-averse, has provided heritability estimates for a wide array of psychological dimensions ranging from IQ and its subscores (visuospatial, verbal, mathematical, etc.), to reaction time, to the “big 5” (e.g. extraversion/intraversion, neuroticism, etc.), to all psychiatric disorders (e.g. autism, schizophrenia), to what brand of cereal you prefer in the morning, and much more. In virtually all cases, these heritability estimates are higher than zero — often substantially higher than zero. They are not only consistent with studies of identical twins reared apart, but also longitudinal adoption studies: studies with sample sizes ranging in the multiple thousands have demonstrated consistently that adopted children, even when adopted during early infancy, resemble their biological parents to a vastly higher degree than they resemble the adults who actually raised them (i.e. “adoptive” parents). [See Taming the “Tiger Mom” and Tackling the Parenting Myth]
And one of the most common, and in fact the overarching application of heritability estimates is evolution. Heritability estimates tell you precisely how much a trait will change in a population, over time, as a response to selection. In other words, if the smallest 25% of all cattle in a herd failed to reproduce every generation, how much would you expect that trait to increase over time? Given even modest selection on any trait from height, to violence, to “visuospatial IQ”, to extroversion, and much more — just about how much heritable variation would you expect see between the disparate human populations on Earth since the time we migrated out of east Africa?
The answer is obvious. if you have read The 10,000 Year Explosion by Cochran and Harpending (which I’m not sure you have), the authors provide ample evidence that substantial heritable change is possible in the relative blink of an eye — hundreds or thousands of years, not just tens of thousands. (Evolutionarily speaking, of course.) It is a trivial matter to ensure that a population, twenty generations from now, will be on average as bright as the brightest 2% within that population today [see The breeder’s equation | West Hunter]. Today’s Scandinavians are not yesterday’s Vikings. Han Chinese in Sichuan Province today are not genetically exchangeable with Chinese during the reign of the first Qin Emperor. Swedes are not Norwegians, Egyptian Copts are not Muslims, and Hejazi Arabs are not Najdi Arabs. I could belabor this point ad nauseam, but I believe I have made my point sufficiently clear.
Of course, this is not to say that all of the variation in behavior you see among human beings is hereditary in origin. Nobody ever claimed that — a heritability estimate below 1.0 proves some source of variation that is exogenous to the germ plasm, or perhaps a statistical artifact that is generated in the process of (imperfectly) measuring the trait in question.
Now, on to some specific points you made in your post:
3) You also misrepresent some of the basic claims of some of the bloggers in the HBD sphere. HBD-chick, for one, who does a lot of blogging about consanguineous marriages and its implications for human evolution. You claim:
That account also makes bizarre claims, like the idea that altruism is greater in societies that have complex marriage systems and that ‘marry out’ of the family unit – because, apparently, when you marry out of your circle for generation after generation, everyone you meet is almost guaranteed to be your relative and therefore worthier of compassion!
No. The point is that human populations vary considerably, throughout the ages, in the degree and prevalence of consanguineous marriages, and that basic arithmetic would show you that this will increase the relatedness of two members within an extended family beyond what may be expected from random mating. The Gulf Arabs have been marrying their cousins for centuries, and this practice possibly dates earlier than the prophet Muhammad — Norwegians and Danes haven’t. This means that Saudis, on average, are much more inbred than your typical northern European, and that this difference can be measured through segments of DNA that are “IBD” (identical by descent) — Arabs share a lot more of these than ethnic groups where cousin marriage is taboo.
The coefficients of relatedness work somewhat like this: normally, your brother shares half of your DNA that is identical by descent, as do your biological parents. Your nieces and nephews share 1/4. Your cousins share 1/8. So on, and so forth. Hamilton’s laws demonstrate altruism (e.g. reducing your own fitness, on the behalf of someone other than yourself) can boost an organism’s fitness, on average, if the recipient of the altruism increases its fitness in a way that is commensurate with the relatedness of the altruist and the recipient. In other words, rB > c.
Imagine that by sacrificing your life to save your brother who is drowning, you thereby ensure that your brother would have three additional children that he would not have otherwise had, had he been permitted to sink (and drown). On average, this would ensure a net benefit of fitness for yourself, despite the fact that you have totally abandoned the carrier of your genes (your body) by sacrificing yourself on behalf of your brother. Why? Because 3 multipled by 1/2 (the fraction of genes that your brother, on average, shares in common with you) is greater than 1. You will have increased your contribution to the gene pool. And any alleles that promote such an altruistic behavior on behalf of a person, for his blood relatives, should increase in frequency through selection [see inclusive inclusive fitness | hbd* chick]. This is especially the case for populations that have been inbreeding throughout the ages — because brothers, in this circumstance, are more related to each other than ordinary brothers. [See technical stuff | hbd* chick]
The idea is that this sort of consanguinity would increase the fitness rewards for altruism on behalf of blood relatives to an unusually high degree that is absent among populations that have been out-breeding. In other words, it increases the odds of nepotism, clannishness, and feuding between clans, among other anti-social behaviors that make a civil society very difficult, among other destructive consequences. (Without peeking, who is more likely to help his brother cheat on a standardized test to qualify for a job — the average Najdi Arab, or the average Finn?)
For societies that have been deliberately outbreeding, the exact opposite scenario occurs — distant relatives, whether you realize it consciously or not, are more related to you than they would be in a society with perfectly random mating, and hence you see higher levels of the low-degree altruism that makes the sort of society you see in Woebegon Lake or Sweden possible. The idea is that Swedes are much more willing to sacrifice their fitness in a modest way on behalf of complete strangers who are members of their ethnic group, e.g. by paying higher taxes, and that this tendency has been selected for since the introduction of Christianity during the medieval era, which forbade consanguineous marriages throughout much of western Europe [see setting the stage? | hbd* chick]. Like I said earlier. You only need hundreds of years to see a noticeable change.
If you remain skeptical of this theory, all is fine, but let me tell you something — it does a decent job explaining why the Swedish welfare state works perfectly fine for Scandinavians, but results in utter dysfunction for Somali refugees. It explains why democracy persistently fails in certain parts of the world, despite billions of dollars spent on aid, foreign advisers, and the best advice of seasoned policymakers — some people don’t give a damn about people outside their extended family, and you can’t change that. It explains why there is a west-east cline in Europe for corruption, social trust, and civic mindedness, inasmuch as they can be measured by political scientists — Ukrainians are much more corrupt than the Norwegians, and they’ve been this way for a long time [see big summary post on the hajnal line | hbd* chick]. It does NOT say that all human behavior is [completely] genetically mediated, or that altruism is automatically greater in societies were people have been marrying unrelated persons. Which is why one or two generations of marrying more distant relatives – or marrying outside the group entirely – won’t produce a substantial change in a people’s behavioral traits. Long-term selective pressures are necessary [see this comment of mine].
Being invaded doesn’t explain why you suspect that your neighbor might rob you if he thought he could get away with it (and of course, your suspicions are valid). It doesn’t explain why, if a friend of yours ever lands any sort of government job, he instantly uses it as a mechanism to rip off other people, and to instantly hire dozens of his unqualified relatives and near-relatives. It doesn’t explain why you can’t get anything done in your neighborhood without paying a thousand bribes, from obtaining a drivers’ license to calling the police in the event of a home intrusion.
Poverty doesn’t explain this well, either. In fact, you might expect the direction of causality to be in the other direction. Hard to get an advanced economy going when people are constantly at each others’ throats, is it? But I digress.
Both Japan and Germany had relatively low rates of these anti-social behaviors when they were being bombed to the Stone Age by the allies. Compare the coordination of Japanese civilians during the war effort to the bumbling of south Italians. (And thank goodness that at least one group of fascists was incompetent.) These behaviors can be fixed through social institutions, but they don’t work all the way — and you have to get them running in the first place, which can be difficult if people in a society simply do not trust each other at all.
You know something is strange when the descendants of Scandinavian immigrants in America are practicing a variant of Jante Law multiple generations after the first stock of founding immigrants — long after they have forgotten how to speak Swedish or Danish or whatever. It might even make you wonder sometime. Why haven’t the corrupt institutions of America polluted them yet? [See Maps of the American Nations and Rural White Liberals – a Key to Understanding the Political Divide]
Why are members of the Chinese disapora from Malaysia to Peru considered a model minority, no matter what the local circumstances? There’s a wide variation in social circumstances between Japan, Malaysia, Canada, France, Indonesia, and the rest — yet in any case, the Chinese tend to behave more similarly to each other than they do to the local people. Their IQ scores are dead similar, as is their record of academic achievement. (In Malaysia they were imported as poor tin miners and laborers — and yet the Malays need race quotas to restrict their entry into universities.)
You’d think you’d find one place on Earth where a Chinatown looks closer to Haiti than it does to Shenzhen, but you don’t. Culture matters, but invoking it to explain all the commonness you see around you simply defies the imagination.
You might think it makes sense, but I don’t.
You can blame just about X on any Y as long as you find an association between the two variables. But here is what I consider most troublesome about “culture only” explanations. They violate Occam’s Razor in just about every way imaginable.
For instance, how is white supremacy responsible for both higher IQs among Ashkenazi Jews AND lower IQs among African Americans?
How are aerial bombings to blame for the high trust and cooperation among Japanese during WWII, yet be simultaneously responsible for lower social trust in eastern Europe or elsewhere?
Why do economists blame natural resources for the social dysfunction and internecine warfare in the Congo, yet also attribute natural resources to the success of western settler nations? Why do Gulf Arabs and Equitoreal Guineans behave so currently when they land upon oil? The former have actually built a society of sorts, while the latter nation has children staving in the streets despite a per capita GDP in excess of $36,000. Why?
Why is a culture of rabbinical scholarship to blame for higher rates of achievement among Ashkenazi Jews, despite the fact that Mizrahi Jews have a parallel culture and yet much lower IQ scores?
Why do different populations react so differently to “white supremacism, racism, and poverty”? Why do some people respond to extreme material deprivation with high rates of violent crime, and others with low crime? How on Earth does poverty boost the athletic abilities of African Americans (while depressing their academic abilities), if both are largely socially determined, which is a standard opinion among sociologists? How does one go up while the other goes down? How on earth can anyone blame high rates of sexual assault on outsider prejudice? [See Richard Lynn’s The Global Bell Curve: Race, IQ, and Inequality Worldwide, Welcome Readers from Portugal!, and “Racial Reality” Provides My 150th Post]
If a single social variable has very different impacts on two different kinds of people, perhaps it is time to explore alternative explanations.
Various other commenters have left responses to West, including me, Greg Cochran, and Henry Harpending. I’m convinced that A. J. West is only able to selectively acknowledge facts. He is very much like a creationist in that regard. Normally, I don’t bother make commentary about the personal attributes of people I debate with, but West’s seeming highly limited and selective regard for facts demands some explanation. His post was quite useful in that it led HBD’ers to review the basics of why we think the notions that fall under the category of “human biodiversity” are correct, much as creationists do for evolution itself. But then, I’m not the first person to draw parallels between HBD-deniers and creationists (see Will Saletan’s Liberal Creationism).
I do want to make a statement on one of the points that misdreavus brought up, a point of much confusion within the HBD world and without. As I have tired to explain in my earlier post, Environmental Hereditarianism, the behavioral and physical traits of people are environmentally context-dependent. The broad environmental context regulates the expression of the genes. There is not a dichotomy between genes and “environment”. Nor could there be one – we are always “with” both. The broad environment includes geography, climate, technology, and prevailing social landscape (otherwise known as “culture”). When the social-technological-geographic landscape changes, you can have broad behavioral change all without genetic change. This explains secular changes that occur too quickly to be a result of evolution, such as the sexual revolution, the modern rise in irreligiosity, the increase in the obesity rate, etc.
(I know that this will still not sink in with some people, but I repeat it anyway.)
A note about “culture” though – the “social landscape”, or even changes in such, don’t exist in a vacuum divorced from genes. As HBD Chick so often asks, where does culture come from? Culture is itself an expression of the genes. Yes, behavior – and for that matter selective pressures – are affected by culture. Which in turn is affected by the genes. Which affects the culture, and so on. This is the essence of gene-culture co-evolution. Even rapid “cultural” change, such as the much bemoaned (by social conservatives) sexual revolution has a genetic influence. Rapid change can result when an idea receives widespread appeal among the people. Both components of this – the origin of the idea itself (a reflection of the heritable temperament of its progenitors) – and its reception among the masses (a reflection of the heritable temperament of adherents) are influenced by genes. In a way then, social revolutions can reflect pent-up genetic “potential” in a population, which may express itself when enough people accept that the idea is “OK” and hence can successfully overturn the established order. This is the essence of HBD Chick’s ideas, and Staffan’s remark on needing to “account” for the “history of communism” when looking at the current state of Eastern European societies (“We can’t adjust for their entire history”). The sexual revolution wasn’t the only revolution of consequence in relatively recent history. The American Revolution itself, the Protestant Reformation, the abolition of slavery in the U.S., the rise of communism in Russia, etc are as well. Historical revolutions are in essence, in many respects, a “changing of the genetic guard”, where the genetic dam “bursts” so to speak. More loosely attached individuals may convert if the idea attains a critical mass (see how much longer? | hbd* chick).
To be clear: this is not to say that “genetic potential” is the only factor. As mentioned, other realities, such as technology and the geographic/climatic landscape affect the viability of new ideas/behaviors, and facilitate or quench their dispersal. However, we do see the role of bursting genetic potential when new groups fission from earlier ones, such as the Quakers, the Puritans, or the Mormons (who are descended from Puritans). And this leads to my observation (so lamented by A. J. West):
But, as I and others have so tirelessly tried to show, the innate differences between people, between individuals, between the sexes, and between groups, is of paramount significance to explaining the world. Indeed, how could it be any other way? This is like trying to explain chemistry without knowing the properties of molecules, atoms, electrons, protons, etc. Taking heredity and its effects on people is simply science, as is human biodiversity in general. How foolish and intellectually stifling is it for “educated” people to act otherwise.
A couple of interesting stories have come to my attention lately. Despite my efforts to get them across on Twitter, they are still not quite getting the attention I think they deserve, so I’m going to recite them here.
These stories are on the role of sugar and the role of antibiotics in human health. First I’ll start with the one that is more solid, the case of sugar. It’s essentially accepted doctrine that sugar is harmful to health. This ranges from any sugar at all to “excessive” consumption of sugar. Indeed, it’s accepted in many circles that sugar is behind the rise in obesity rates. There’s only one problem: there isn’t actually any good evidence for this.
Let me repeat a point, a point I will keep repeating until it sinks in: uncontrolled correlational studies do not count as evidence.
With that out of the way, let review an interesting post by Anne Buchanan. (Yes, that one. Before anyone makes the accusation, yes, I am well aware of Buchanan’s and crew’s heredity denial. But the expression “even a broken clock…” is a key bit of wisdom to keep in mind. I judge arguments, not people, and so should you.)
The search for magic health bullets, or the Single Evil goes on unabated, despite a steady record of essential failure. Is that fair? Well, we’ve got decades of very extensive, expensive, and expansively technical studies of some questions of major public health relevance — and little to show for it.
As a new example, after a two-year effort to connect the dots between between sugar and disease, the World Health Organization, whose large professional research staff should know how to do that, believes it has done so, and now recommends we all reduce our sugar intake to 10% of our diet, or better yet, 5%. That’s 12 or fewer tablespoons of sugar a day.
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To answer that question, the WHO commissioned a meta-analysis, that is, a single combined analysis of all pertinent previous cohort studies of the effects of sugar on obesity, which was published last month in the British Medical Journal by Morenga et al.
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That is, people in these studies were either asked to add or subtract sugary foods and drinks from their diet, but change nothing else, or they were asked to subtract sugar and substitute it with a different carbohydrate. Presumably the latter was to control for the effect of simply adding or subtracting calories of any sort, though this isn’t clear in the paper.
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From these 30 trials and 38 prospective cohort studies, what do they conclude? Well, of the 30 trials, five studies measured the effect of reducing dietary sugars. To quote the authors of the WHO commissioned BMJ paper, “Reduction in dietary sugars intake was associated with significantly reduced weight (-0.80 kg (95% confidence interval -1.21 to -0.39); P lt 0.001) at the end of the intervention period by comparison with no reduction or an increase in sugars intake.”
So, five studies report statistically ‘significant’ weight loss with reduction in sugar intake. But what are we talking about here? Well, an average decrease of less than 2 pounds, or at most 2 1/2 pounds, with variation around that. This may be ‘statistically significant’, but all I can say is that if I lost 2 pounds I wouldn’t think it important enough to tell my mother about, never mind publish it. And, only one of the studies, participants were asked to substitute low sugar foods for the high sugar foods they were eliminating. So, one study tried to test the effect of eliminating sugar, but not changing caloric intake, but the others did not.
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So, after all of this effort, on a subject that has been widely trumpeted as well-known, is sugar bad for us? Maybe, but we don’t know it from this study. All the studies included in the meta-analysis are based on methods of assessing food intake that are themselves questionable. Dietary recall, the method used in the trials, and food frequency questionnaires used in the cohort studies, or indeed just about any other method of dietary assessment, are notoriously inaccurate measures of what we eat. And, the amount of weight gain reported to be due to sugar consumption is perhaps statistically significant, but with respect to the dangers associated with obesity, it’s trivial.
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All of this is predicated on the assumption that weight gain is unhealthy. Or leads to ill health. The WHO paper didn’t address the strength of the evidence for this. Nor did they show any evidence to suggest that sugar contributes to ill health, or even weight gain, any more than any other food. When speculating on how sugar could be associated with weight gain, the authors write, “The most obvious mechanism by which increasing sugars might promote weight gain is by increasing energy consumption to an extent that exceeds energy output and distorts energy balance.” That is, people who gain weight consume more of anything than they burn, as the isoenergetic studies suggest. By this logic, eliminating milk or eggs or meat and not replacing them would cause weight loss, too.
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Sugar consumption is much less unambiguously associated with tooth decay. Or at least I thought so, and it seemed something ‘everybody knows’…..until I read the review commissioned by the WHO, a paper in the Journal of Dental Research, the foundation for the WHO recommendation that sugar consumption should be less than 5% of our diet.
From 5,990 papers identified, 55 studies were eligible – 3 intervention, 8 cohort, 20 population, and 24 cross-sectional. Data variability limited meta-analysis. Of the studies, 42 out of 50 of those in children and 5 out of 5 in adults reported at least one positive association between sugars and caries. There is evidence of moderate quality showing that caries is lower when free-sugars intake is < 10% E. With the < 5% E cut-off, a significant relationship was observed, but the evidence was judged to be of very low quality. The findings are relevant to minimizing caries risk throughout the life course.
The evidence for an association is judged to be ‘moderate’ or ‘of very low quality.’ This largely reflects the fact that most studies didn’t ask the question the WHO was interested in — is there a threshold amount of sugar that is highly associated with cavities? Still, the studies do show an association, even if confounders like socioeconomic status might be problems.
Buchanan seems to be channeling many criticisms I have made, as I did in a Twitter discussion I once had with John Durant. The commonly held belief that sugar per se leads to ill-health – even the most basic (and commonly accepted) link in the case of tooth decay – isn’t based on any good evidence. That sugar is the cause of the rise in obesity is also commonly believed, but is not substantiated.
Notice that sugar is notoriously absent from Greg Cochran’s discussion of health problems stemming from poor adaptation to evolutionary novel foodstuffs (Death by Chocolate | West Hunter). Odds are people looking at sugar are looking in the wrong place.
What should they be looking at? This brings me to antibiotics. Apparently, antibiotics reliably leads to weight gain in animals:
IF you walk into a farm-supply store today, you’re likely to find a bag of antibiotic powder that claims to boost the growth of poultry and livestock. That’s because decades of agricultural research has shown that antibiotics seem to flip a switch in young animals’ bodies, helping them pack on pounds. Manufacturers brag about the miraculous effects of feeding antibiotics to chicks and nursing calves. Dusty agricultural journals attest to the ways in which the drugs can act like a kind of superfood to produce cheap meat.
Now, of course, I am a huge critic of generalizing from animals to humans. However, the article does mention that at least one human trial was conducted:
Researchers also tried this out in a study of Navy recruits. “Nutritional effects of antibiotics have been noted for some time” in farm animals, the authors of the 1954 study wrote. But “to date there have been few studies of the nutritional effects in humans, and what little evidence is available is largely concerned with young children. The present report seems of interest, therefore, because of the results obtained in a controlled observation of several hundred young American males.” The Navy men who took a dose of antibiotics every morning for seven weeks gained more weight, on average, than the control group.
Unfortunately, time is often lacking for me. I suppose if I dug more deeply (which I may still do at some point), I could turn up evidence that could more definitively establish, yay or nay, on the role of antibiotics in human obesity. However, for now, I will put this out there as an idea that needs further attention. Attempts to nail down the cause of the rise in obesity have been infamously unsuccessful. Part of the investigation has been handicapped by the fact that diet and exercise are assumed to be the ultimate causes. This is far from clear at the moment. I don’t know if antibiotics will hold up as a potential cause either. I am not claiming to know the method that antibiotics plays this role (whether they, for example, alter the composition of the gut microbiome). However, I do believe this is worth closer attention.
For sugar and antibiotics, an interesting irony exists. One is commonly believed to be behind poor health and obesity, and in fact may not be. The other an agent that has legitimately been instrumental in improving human health, but may have the side effect of fattening us up. The laser-like focus on lifestyle has served to make us more paranoid about health, but what do we have to show for it? Not much, as previously discussed in my posts on the matter (Trans Fat Hysteria and the Mystery of Heart Disease and Even George W. Bush Has Heart Disease). Of course, we are likely to run into trouble with antibiotics soon anyway (see Imagining the Post-Antibiotics Future)…
…but that’s a whole ‘nother problem entirely. It would be helpful if modern research would break free of its sociological determinism and hence do a better job at finding what truly ails us.
EDIT: As an example of a worthless correlational study, I present this meta analysis published in the journal PLOS ONE of observational studies looking at birth by Cesarian section versus vaginal delivery and later obesity. It found that babies delivered by C-section were more likely to be obese as adults. It’s an example of the best and baddest of correlational studies. Did even one of those studies control for parental obesity? Doesn’t look that way. Did any of them try to look at differences between siblings where one was delivered vaginally and the other by C-section? Nope. It is a completely worthless study; all it shows is that obese people may be more prone to give birth via C-section – with no idea of the true causes or best correlates at least. Yet, it is being circulated as if it was definitive proof. Give me a break.
Post updated, 9/13/14. See below!
I haven’t always made it explicit, but some of you might gather that I am rather hard on most “environmental” explanations. You have inferred correctly. The reason? Several, which I’ll review here. The biggest of these? There is no good evidence for the vast majority of them.
That’s right, there is little evidence linking most “measurable” aspects of the environment to human physical or behavioral traits. And on this point, it’s important to note that poorly controlled correlational studies (which make up the bulk of the commonly touted evidence for most environmental explanations) are not, by and large, evidence for environmental impact. Most of the solid evidence we do have for environmental impacts come in the forms of things that do physical damage (e.g., maiming limbs or traumatic brain injury) – a category which includes poisons; or are developmental deficits, such as malnutrition. Much of the rest of it (take your pick) is lacking.
Let me be clear: “strict” hereditarianism – that claims human traits are “all in the genes” is wrong.
Oddly, the impact of pathogens – particularly behavioral impacts such as the previously discussed gay germ hypothesis of Greg Cochran – is amongst the most solid known examples of true “environmental effects” – in this case, on a behavioral trait. The paper referenced in that post explained that pathogens may be a significant force behind variation in health and behavioral outcomes.
This paper, by Cochran & Ewald, noted that even many “physiological” outcomes, such as health, can’t reliably be pinned to environmental sources. So much for power of lifestyle!
A good bit of this was discussed by James Thompson in his post Diet is an IQ test. Contra what we’re told, we simply don’t have reliable evidence for environmental impacts on health outcomes or behavioral traits.
You may now be wondering what’s this about not thinking heredity is “all there is” after what I’ve just said. Allow me to clarify my position, and in so doing consolidate some of my recent comments on the matter.
See this comment of mine at HBD Chick’s (emphasis not in the original):
Behavior, and more broadly behavioral traits are environmentally context-dependent. This is a fine point that many, conceptually, fail to fully grasp. The reason why this is so is mainly because the socio/cultural/technological landscape of the day sets the playing field. People with different genetic predispositions have to adopt different tactics depending on what works; they receive a different set of incentives and feedback to their behavior [depending on the socio-technological landscape of the day]. Obviously, some people play the game of the day better than others. This is what sets up selective forces every society exerts. Of course, when the landscape changes, behavior can change over all, and who has the advantage changes.
The effective landscape explains how you can get rapid changes in behavioral traits all without comparable genetic change. As you say, the rise in irreligiosity, increasing acceptance of same-sex marriage, etc, are examples. This confuses many people, because they somehow assume that if you can have rapid environmental change on behavioral traits, that they can’t be so “heritable” after all (despite the fact that they all are). This stems from the misconception that heritability = degree of mutability, which is wrong. Average height for example has increased considerably in America over the past century (after decreasing for some time), and virtual no one then claims that height is “less heritable” than we thought because of this. The rise in obesity is another example. Some take the increase to signal that environment is much more important that it is let on.
Of course, these people mean “environment” in the sense of the environment that differs between people living today, where is the change over time was brought on by an environmental change that (in a fashion) affects everybody. The playing field is different. But that knowledge doesn’t necessarily guide you in how to change it, or if an effective change is even possible.
I’m not sure if that helps to clear up the issue for those confused about it, because it is admittedly a difficult concept to grasp.
This is a key fact that underlies my thinking, but doesn’t seem appreciated in the minds of many. The strongest evidence for some sort of environmental impact is broad secular changes in behavioral or physical traits that occur too fast to be the result of genetic change, i.e., evolution. This occurs because one’s genome unfolds in the environment it finds itself in. A change in the environment might alter the outcome of the genetic programming. Of course, this doesn’t mean that anything goes. We don’t open the door to any old environmental theory because of homeostasis. The genes are designed to produce a working copy of the organism despite a temperamental environment. The genetic code is built in with buffers that keep development on track. This is not exactly a perfect process (and some individuals’ buffering seems to work better than others), but it is a key phenomenon to keep in mind.
This also doesn’t mean that because this process occurs, we can necessarily isolate the aspects of the environment that brings about these secular changes. Often, we can’t. Two poignant examples (and two big ones in the “Dark Enlightenment” sphere) are marriage/mating behavior (i.e., the decline in marriage rates and rise of unwed motherhood) and the rise in obesity rates. In both cases, we don’t know for sure what the causes are, even if we think we have ideas about them. This is especially so in the case of obesity. Determining the causes with any certainty is difficult.
Going beyond the difficulty of isolating a cause of secular changes, assuming one even knew what theses causes were, knowing that changing an environment could affect people’s outcomes in principle doesn’t mean that it’s always possible to make the necessary changes in practice. This may ultimately prove to be a mistake, but I’ll leave it to readers for now to figure out why this is so.
OK, but that’s the grand-scale environment, the world of difference, so to speak. What about individual differences? What about that “nature and nurture” mantra we’re often fed by behavioral geneticists and others on the matter? Well, turns out that’s a bunch of bullshit too. See the post on the matter over at HBD Chick’s, it’s not nature and nurture…, where she quotes Steven Pinker (HBD Chick’s emphasis):
“Even the technical sense of ‘environment’ used in quantitative behavioral genetics is perversely confusing. Now, there is nothing wrong with partitioning phenotypic variance into components that correlate with genetic variation (heritability) and with variation among families (‘shared environment’). The problem comes from the so-called ‘nonshared’ or ‘unique environmental influences.’ This consists of all the variance that is attributable neither to genetic nor familiar variation. In most studies, it’s calculated as 1 – (heritability + shared environment). Practically, you can think of it as the differences between identical twins who grow up in the same home. They share their genes, parents, older and younger siblings, home, school, peers, and neighborhood. So what could make them different? Under the assumption that behavior is a product of genes plus environment, it must be something in the environment of one that is not in the environment of the other.
“But this category really should be called ‘miscellaneous/unknown,’ because it has nothing necessarily to do with any measurable aspect of the environment, such as one sibling getting the top bunk bed and the other the bottom, or a parent unpredictably favoring one child, or one sibling getting chased by a dog, coming down with a virus, or being favored by a teacher. These influences are purely conjectural, and studies looking for them have failed to find them. The alternative is that this component actually consists of the effects of chance – new mutations, quirky prenatal effects, noise in brain development, and events in life with unpredictable effects.”
Here she continues, quoting me on the matter (HBD Chick’s emphasis):
“The heritability of behavioral traits is typically on order of 50%. However, what’s left (after you subtract the ‘shared environment’, which is generally 0, but more on that soon) is just the ‘unexplained variance.’ We don’t know what that is. Much of it, perhaps a good deal, is measurement error. Evidence suggest that that is actually missed heritable influence.
“However, what’s left over, after you’ve accounted for ‘attenuated heredity’ may be what’s known developmental noise. This is ‘environmental’ in the sense that it’s not inherited, but is essentially random and not subject to controlled manipulation.
“Or we think it’s random. See Kevin Mitchell on it:”
.
“Even developmental noise appears to heritable, to a degree. Whether or not this is ‘on purpose’ or an evolutionary accident is unclear.[Edit, 9/13/14: And now we have additional evidence that this is the case. Experiments on multiple strains of genetically identical fruit flies have found that some strains are more prone to having variable trait expression despite an identical genotype than are others. The range of variation is itself influenced by the presence of certain genes. Additionally, these genes don’t seem to allow for greater variation across the board, but rather, greater phenotypic variation in specific traits. In short, the degree of variation, in the case of humans, between identical twins, may indeed be a function of the genotypes of those twins. See Ayroles, et al, 2014]
“And finally, and this is an ‘advanced’ topic, impact of the ‘unique environment’ – what makes identical twins raised together different from one another – could itself significantly genetic in nature, because identical twins aren’t actually genetically identical, but have different de novo mutations.
“You see why I’m a little hard on the ‘nurturists’ out there. Broadly, the evidence has not been kind to ‘environmental’ influences. Note that this is not to say that they don’t exist.”
About that 50-50 split, I noted that much of the 50% not ascribed to genes is in fact measurement error. Staffan had a post on that matter (emphasis added):
So, what does the “new” research from the 1980s, that is now finally beginning to reach public awareness, tell us about human nature? The most obvious part is that nature is a major factor. This is typically summed up in textbooks in the 50/50 rule, claiming that genes and environment can explain about half of the variance each of things like intelligence, personality, psychopathology etc. Which is easy to remember – but also incorrect. This is due to the fact that there is something called measurement error. Most studies are done in a way that doesn’t distinguish this error from the environmental factor. So it’s 50 percent nature and 50 percent environment plus measurement error. Studies that have managed to minimize measurement error typically yield heritabilities for personality traits and similar characteristics around 70 percent. You also have the fact that some of the traits linked to the most important life outcomes, like intelligence and impulsiveness, have even higher heritabilities, around 0.75-0.80.
Here’s a quote from the abstract of one of these studies Staffan mentioned (emphasis mine):
Our analysis of self-report data replicates earlier findings of a substantial genetic influence on the Big Five (h2= .42 to .56). We also found this influence for peer reports. Our results validate findings based solely on self-reports. However, estimates of genetic contributions to phenotypic variance were substantially higher when based on peer reports (h2= .51 to .81) or self- and peer reports (h2= .66 to .79) because these data allowed us to separate error variance from variance due to nonshared environmental influences. Correlations between self- and peer reports reflected the same genetic influences to a much higher extent than identical environmental effects.
And of course, there is one additional factor, something that’s greatly under-appreciated (because it’s inconvenient for researchers) but is likely very powerful. Quoting myself from over at HBD Chick’s (emphasis in original):
And finally, perhaps most poignant of all, but greatly underrated, is the fact that that identical twins are not actually genetically identical, but possess subtle differences due to de novo mutations. While behavioral geneticists and others like to ignore these, identical twins are our metric of the effects of heredity. We think we can precisely measure the genetic effect vs “environmental” one by looking at identical twins raised together – anything different between them must be due to environment, so the story goes. But the differences between them could be due to genes, so in reality, we have no idea how big the effect of the “environment” truly is.These differences are starting to recognized as being potentially powerful, as seen from the differences of supposedly (but not truly) genetically identical mice:
All mice are the same, until they’re not | Science News
Genetic tests that can distinguish between identical twins are becoming availible. This is an underappreciate goldmine in future research into genes and environment.
There’s a dude over at Steve Sailer’s that was trying to argue with me about this key point. He’s trying to claim that since most mutations are of neutral effect, we can ignore these subtle genetic differences between identical twins. Well, the mouse studies indicates that we can’t. Tiny genetic differences can lead to large differences in expressed traits. This has practical significance up and down the board. For one, it does cast into question the wisdom of assuming twins are perfect genetic control in observational studies (as I said to Staffan, the genetic confound never goes away).
This post is a teaser because I plan a longer, much more thorough post on the topic soon. However, I wanted to summarize what I have said on the topic so far. The key problem with recognizing the true pervasiveness of heredity and the relative insignificance and capriciousness of the environment is that it makes it all the more difficult to craft a better a world. This isn’t a problem for only the blank-slatist types. The HBD-aware often share these hopes. Many in this space leave the door open for the environment in the hopes that we can engineer better outcomes if we try (not just harder, as utopian liberals believe, but, perhaps smarter as well). From, parenting, to lifestyle, to social engineering, unfortunately, it turns out, the reality is not so simple. There isn’t always something you can do. The truth calls for a type of serenity – accepting what you cannot change. Perhaps this makes heredity an even harder sell than it is, but in all our marketing, we (or at least, some of us) have to be sure we aren’t sacrificing the truth in the process.
EDIT, 5/1/14: Looks like my comment did finally appear, buried among over 500 others.
Comment moderation is an understandable practice, but at times it is rather annoying, especially when it’s used for less than above-board purposes. I left a comment to Jared Taylor’s review of Nicholas Wade’s forthcoming book A Troublesome Inheritance: Genes, Race, and Human History. My comment has yet to emerge from moderation, and other, newer comments have, suggesting that it may never do so. This is much too an important issue to wait, but fortunately I have a blog, so here is my comment:
Interesting, it’s good to finally see a review of this book.
I’m glad Wade is trying popularize this topic, giving it its much-needed due. In so doing, however, he has, as I expected, gotten quite a few things wrong. Unfortunately, those things that are wrong will be remembered more than the corrections to them.
DNA studies show that Tibetans split off from Han Chinese only 3,000
years ago, so it must be only since then that Sherpas evolved their
ability to function so well at high altitudes.Though this latest evidence is probably too new for Wade to have included it in his book, that’s not exactly true. The Sherpa adaptation goes back much longer than that. The Tibetans are a fusion of a Han-like population and a Sherpa-like population, who picked up their high-altitude adaptation from the latter group. See Greg Cochran on it:
A novel mechanism for getting high | West Hunter
One of Mr. Wade’s lesser breaches of good manners is to note that Europe made crucial breakthroughs in civilization that many groups have yet to adopt: “Europeans, probably for reasons of both evolution and history, have been able to create open and innovative societies, starkly different from the default human arrangements of tribalism or autocracy.”
Academics have long chased their tails trying to explain why some countries are rich and others poor. Mr. Wade points out that their fatal blunder is to assume that all populations are interchangeable. He uses findings by the economic historian Gregory Clark to suggest that in Britain, where records go back far enough to make such studies possible, there was steady evolution towards the qualities crucial to the Industrial Revolution.
I hope Wade also realizes that just as not all human populations are interchangeable, not all Europeans are interchangeable. Nor, for that, matter, are all White Americans interchangeable.
Mr. Wade’s discussion of the MAO-A gene is even more contortionist. He concedes that American blacks are no less than 50 times more likely than whites to carry the variant most closely tied to violence, but says we must draw no conclusions: Whites might have different, as yet undiscovered, alleles that would make them just as violent.
Many Blacks apparently do indeed possess versions of MAO-A that have been linked to higher aggression:
How Much Hard Evidence Do You Need? | JayMan’s Blog
That’s not possible. If human differences have “far reaching implications” there is no way to “dispel the fear” of what goes by the name of “racism.” What, to begin with, are these far reaching implications?
…
The liberal façade is all of a piece. It cannot be punctured only in a few safe and convenient spots. That is why its guardians plug every chink with such bloodthirsty zeal. To accept what dissidents call human biodiversity would open the door to everything the regime most piously hates: immigration control, inequality, self-segregation, nationalism, mono-culturalism. Whether he knows it or not, and no matter how hard he denies it, Mr. Wade has taken a match to the entire liberal/modern world view. The next thing you know, someone might say the Civil Rights Act of 1964 should be repealed or that women have no business on submarines.
Perhaps those things are indeed an inevitable conclusion of society openly embracing HBD, as I have discussed before. These might represent not unwarranted reasons to be concerned about public acceptance of this knowledge. I am of the mind that these things not be inevitable conclusions, but some of that will indeed come up. The extent that it does will be itself dictated by the mindsets of the people who discuss it, which itself explained by HBD (see above about White Americans). This is a serious issue that, if true, might represent some real justification for liberal reticence about HBD.
In this post, I will review Gregory Cochran’s “gay germ” hypothesis. I wanted to make an index of Cochran’s posts from his and Henry Harpending’s blog West Hunter that discuss it. These posts don’t seem to all show up under the “Homosexuality” category there, and I wanted links to them to be all in one place. So here are the key posts, with a brief synopsis of each post’s major points. In reviewing this hypothesis, I cite an earlier paper co-authored by Cochran on the matter, one which discusses the role pathogens may play in all manner of human diseases and behaviors.
The “gay germ” hypothesis is very much Cochran’s, not mine (I haven’t contributed anything to it, except, perhaps, the name). I just believe that it is very likely correct, and promote it. Here is the list:
Depths of Madness – The first post in the series. Here Cochran lays out the basic case, and notes key facts that point to the pathogen (e.g., high rate of discordance between identical twins, the evolutionary maladaptiveness of obligate male homosexuality and the paradox of how it could have become so common, how pathogens can affect brain function)
Paternal Age and Homosexuality – Explains why genetic load (burden of accumulated deleterious mutation) can’t explain the existence of male homosexuality, especially at its relatively high prevalence. Notes that unlike afflictions that likely are caused by genetic load, there doesn’t seem to be increased incidence of homosexuality in the children of older fathers.
Group Selection (and homosexuality) – Why group selection (multi-level selection) of the type proposed by E.O. Wilson doesn’t work in general and why it certainly can’t explain male homosexuality. Debunks the “gay uncle” hypothesis.
Homosexuality, epigenetics, and zebras – Why developmental noise, including in-utero epigenetic modifications, cannot explain male homosexuality (in short, natural selection has a strong incentive to prevent low-fitness phenotypes from manifesting, so such congenital defects are all rare)
Heads exploding – The introspective post. Appropriately titled, Cochran invites discussion on the social and scientific consequences of nailing down the biological cause of homosexuality – any cause, regardless if that turned out to be the pathogen as he suspects. (As we’ve seen, public discussion of any biological determinant of homosexuality will have consequences, and as I’ve discussed, not necessarily good ones.)
Math is Hard – Rips on E.O. Wilson, and innumerate social scientists in general, who are largely unable to quantitatively evaluate their variously kooky hypotheses (as I’ve said elsewhere, “everything, and I mean everything, can be quantified”). Dishes on Wilson’s “gay uncle” hypothesis as example of these, one of many other nonsensical notions in social science.
Hamilton Rules OK! – Reviews the mathematics of kin altruism (Hamilton’s rule), and again notes why “gay uncle” type altruism doesn’t work.
Not Final! – Key post where Cochran reviews the case for the gay germ, demonstrating the unworkability of all the alternatives. Shows how processes of elimination (essentially, the reductio ad absurdum) can sometime be a useful method of getting at the truth. Excludes ideas such heterozygote advantage (requires very strong selective pressure for advantage – but nonetheless ruled out by GWAS), sexual antagonistic selection (i.e., benefit to females but costly to males – also ruled out by GWAS), group selection (impossible, and no evidence anyway). Explains the how immune complexes generated by molecular mimicry can cause damage to specific tissues not infected by the pathogen. Notes the ubiquitous impact of genes, but the often highly indirect nature of this impact, which may explain the low but non-zero heritability of homosexuality. And notes that pathogens are often responsible for common fitness-reducing syndromes.
Biological Determinism – Cochran references yours truly as he talks about the pervasiveness of heredity in all things (i.e., All Human Behavioral Traits are Heritable), with illustrative anecdotes about twins. Notes the role that genes play in infectious diseases, illustrating that they are often a necessary but not sufficient component of the outcome in question – i.e., you must invoke pathogens to explain something like tuberculosis. Such is the case with male homosexuality.
Evolution of Virulence – An in-depth discussion of the evolutionary pressures that lead to the insidiousness of pathogenic organisms. In particularly, notes that since pathogenic organisms’ populations are immensely large and their generation times are so short, they evolve far faster than their hosts could ever hope to. Discusses Trojan Horse pathogens, those that try to hide from their hosts’ defenses by mimicking host molecules, and why these selection on these types of infectious agents tend to favor late-appearing illnesses.
The case for the gay germ is somewhat indirect, but very strong. Critics often level the charge that there is “no evidence” for Cochran’s hypothesis – i.e., that the offending pathogen has yet to be identified. But the claim that there is “no evidence” isn’t really true; there is in fact plenty of evidence. The facts are certainly consistent with a pathogenic explanation, even if we don’t have the pathogen itself nailed down. But, the most compelling evidence comes in the form of ruling out potential alternative explanations. This itself is a form of evidence. The Sherlock Holmes quote, “when you have eliminated the impossible, whatever remains, however improbable, must be the truth,” is an excellent guiding principle, and is certainly valid here. As I’ve said before, there is something to be said for explanations, that, while maybe not conclusively proven, have the virtue in that they lack meaningful competition. This perhaps one of the clearest examples.
Now, I honestly shouldn’t even have to say this, but let me state clearly that I have nothing against gays, I actually do have several gay friends. Quite often (not all the time, but more than a few times), when I discuss Cochran’s hypothesis, I’m accused of being homophobic. It’s very much a knee-jerk reaction. But, as a friend told me yesterday:
you can come across as harsh and I’m learning that to connect with the mainstream, you must tell them that 2+2=4 before you can tell them 4+2=6. If you don’t make the effort to tell them you’re not evil in each post you write, if it’s the first post they’ve read, they’re going to want to think you’re evil, because everyone wants to think that everyone else on the internet is 1) evil and 2) wrong.
…and then some – an unfortunate reality in these situation. This is especially interesting considering that one of the biggest proponents of the gay germ hypothesis, “misdreavus” (whose colorful commentary was featured in my previous post – and whose comments over at West Hunter have added invaluable insight to the gay germ model) is himself gay. How does that compute?
But biggest of all is that the gay germ model is suggestive of the poorly researched role that pathogens can have in some many other areas, both in illnesses and behaviors. Indeed, the of mode of action of Trojan Horse pathogens which rely on molecular mimicry could be responsible for many low-heritability, late-onset diseases, such as Alzheimer’s disease and cancer. Indeed, in the case of cancer, some are known to be caused by infectious agents, such as those caused by the human papilloma virus (HPV) (e.g., genitoanal cancers) and stomach cancer (apparently caused by Helicobacter pylori). As Paul Ewald (Cochran’s co-author on the paper on this matter) explains, as much as 80% of all cancers will turn out to be caused by infections. This would be revolutionary, if true, because it would suggest that there’s a way to fight the often highly unsuccessful war against cancer, as demonstrated by the success of the HPV vaccine.
Their paper discussed the under appreciated role of infectious agents in all manner of human diseases in great depth:
Infectious Causation of Disease: An Evolutionary Perspective (2000)
They note that infections have fallen out of favor as a possible cause of disease because infectious agents have been increasingly harder to identify – many of the easy-to-spot infectious agents have already been found. This leaves the harder to find pathogens to make up the bulk of those left to be discovered.
Indeed, their paper is very insightful, and quite chilling. They note that even many diseases with known genetic links may have infectious roots. Infectious agents may create a selective pressure favoring otherwise deleterious alleles to persist.
Their analysis breaks it down:
One useful tool for diagnosing infectious causation can be derived from the central principle of evolutionary biology: evolutionary fitness. Estimates of the fitness costs that are attributable to a particular disease (averaged over the entire population) can be used as an indicator for assessing whether the disease could reasonably be ascribed to genetic as opposed to infectious causation. For a genetic disease to be maintained at equilibrium in a population, the loss of the allele for the disease must equal the rate at which the allele is reintroduced. If the allele does not provide a fitness benefit, the loss due to the fitness costs of the disease would need to equal the rate at which the allele is generated through mutation. This reasoning leads to the conclusion that estimates of fitness costs can provide a sense of whether the disease is attributable to something other than simple genetic causation. Any human disease with a frequency that is too high to be maintained by the mutation rate is implicated as being caused by something other than just human genes. If the disease is inherited in Mendelian ratios and is too widespread to be accounted for by founder effects or genetic drift, and if the time has been sufficient for natural selection to drive the frequencies of deleterious alleles to low levels, the allele must have conferred some compensating fitness benefit. The only such compensating fitness benefit that has been documented for major human genetic diseases is resistance to infection
Cochran, Ewald, and Cochran note that most cancers – and even heart disease – probably have infectious origins/involvement. Indeed, they lambast the environmental insult (primarily “lifestyle”) explanation for such diseases, noting, (as I have done quite vocally), the failure to reliably establish such environmental causes.
As we’ve seen in my posts on the topic (the whole category of my posts on health, particularly my posts Even George W. Bush Has Heart Disease and Trans Fat Hysteria and the Mystery of Heart Disease), the “lifestyle” causation model of most of these diseases is in pretty poor shape. Cochran et al even argue that even cancers with known environmental causes, like lung cancer, might have pathogenic involvement.
They point out the problem with the current understanding of heart disease:
At a practical level we need to understand the causes of disease to understand how best to decrease the suffering from disease. At a more basic level, as Nesse and Williams have emphasized, we need to understand the causes of disease, because the mix of superb engineering and seemingly underbuilt components in the human body is a mystery. Is a circulatory system prone to atherosclerosis, for example, really like a Mercedes Benz with the soda-straw fuel line? Or is a state-of-the art fuel line simply prone to microbial sabotage? The resolution of this question and the broader set to which it belongs is academic, but it also promises to reorient medical research and may improve fundamentally our states of health.
All these considered, it is rather shameful that researchers in the human sciences don’t take more of a serious interest in the “gay germ” hypothesis (and pathogenic models in general). Objection from non-scientists is somewhat understandable; no one (other than homophobes) wants to believe that gays are literally “diseased”, despite the fact that this is likely true. Here, that statement is merely an empirical one; it contains no value judgement attached to it. However, that scholars haven’t taken an interest in it is simply inexcusable. How patently ridiculous it is that serious thinkers could really believe at this point that any other explanation for male homosexuality is more likely.
As well, as I have noted before, the conventional dogma on homosexuality is an exercise in the purest of ironies. As Cochran put it in his post Against Biology, and as I said elsewhere:
Irony comes in because (obligate homosexual men, who what most are concerned with) were not “born that way” at all, since male homosexuality almost certainly is the result of a childhood infection.
Worse still, homophobia (or homoaversion, as it should properly called, according to Greg Cochran) is itself heritable, at least 54% so. Yes, homophobes were much more “born that way” than homosexuals themselves!
It doesn’t get much more ironic than that.
But the “born that way” meme does speak towards the prevailing attitude towards genetics. Nothing undesirable can be much heritable, for if it is so, it is seen as (not exactly accurately) being immutable. Hence, this is why sexual orientation can be inborn, but IQ, sex, or racial differences cannot.
This is an interesting statement on where we are, intellectually, as a society. Now, I have said that there will likely be some unpleasant consequences if knowledge of the gay germ were to become widespread. At least belief in a genetic cause leaves the promise of a “fix” way off in some uncertain point in the future (when we could say, screen embryos for whatever putative gay genes). However, an infectious origin offers better prospects, giving the hope (well-founded or not) of a more immediate fix, especially if the infectious agent is a virus; it may be prevented with a vaccine.
(As for the question of female same-sex attraction (SSA) – which is likely a completely separate phenomenon from male homosexuality – I will state that my current suspicion is that it likely a side effect of other useful functions. That is, otherwise beneficial genes carried by women sometimes lead to bisexuality. Female SSA appears to be significantly different from male homosexuality. For one, female SSA appears to be continuously distributed along the Kinsey scale, with the majority of non heterosexual women being bisexual. Male SSA, on the other hand, appears to be a more J-shaped distribution. Sexual fluidity seems to be common enough in women that it is a “normal” trait, so to speak. Indeed, I am beginning to suspect that true lesbians do not exist.)
But, even larger than the issue of homosexuality, the fact that pathogens can affect behavior means that they could be a big part of what it is that makes us different from one another – part of the “unexplained variance” – the difference seen identical twins raised together (see it’s not nature and nurture… | hbd* chick). This is an untapped avenue of research that remains to be explored. Now if we could only get that through to the “learned” people…
The diseases that afflict man, from homosexuality to cancer and heart disease, could be the result of nasty organisms that infiltrate our bodies and minds and attack from within. That pathogens could affect so much shouldn’t seem so bewildering, considering that our world is utterly awash in microorganisms. But no, researchers have been instead been generally wasting their time pursuing “lifestyle” as the main explanation for these illnesses (except in the case of homosexuality, as noted above). For some, mostly liberals, the belief that lifestyle is the root of our ills serves to give hope – hope that the things that ail us can be vanquished if we just get people to “eat better and exercise”. For others, mostly conservatives, the belief that the diseases of civilization are self-inflicted justifies haughtiness – giving one license to look down on the sick for their supposedly inferior lifestyles. It’s a tragic state of affairs.
Edit 6/12/14: See also the discussion in the comments here: Noli Irritare Leones » The Germ of the Gaps
The theme for this post is a cue from the original Robocop, something which I feel fits the tone of this post…
Courtesy super-commenter “misdreavus“, over at West Hunter:
let me point out that with notably few exceptions, so-called “HBD” (or “human biodiversity”) is a movement that exists largely within the confines of the internet. This, of course, has done absolutely no favors to its dispersal within society at large, because if technology has taught us anything, it is that the anonymity of the web tends to bring out the crazy and stupid in everyone, Surely there was a time when people actually tried to research certain topics before launching a slurry of half-baked and inchoate opinions with an audacious (and entirely unwarranted) degree of self-confidence — not so much because people were any better informed in yesteryear than they are today, but because certain structural barriers posed an impediment to the crazy and incompetent expressing their ideas in lofty places. Now that (most of) these have been safely dismantled, we’ve got nutters from Stormfront sparring tête–à–tête with anthropology professors over elementary facts that anybody can look up in a linguistics textbook. How splendid is that.
This is a most sudden and hilarious change of affairs. Thanks to the almighty web, we’ve got “white genocide” nutters, “red pillers”, devotees of Asatru, Sedevacantists, keyboard warriors, “neo-reactionaries”, social justice warriors, 4chan experts, and bedlamites of every stripe and fashion littering the comments section of every blog about human biodiversity. [JayMan: and we sure do!] They’re not only shockingly ill-mannered and coarse, but many of them have yet to absorb all of the facts about “HBD” that have been settled science for several decades — you try explaining to any of these “Dark Enlightenment” lunatics that single mothers are not responsible for adverse outcomes in bastard children, as is proven by a wealth of longitudinal adoption studies.
I can’t decide whether or not I like it at all, for the life of me — but it’s here to stay!
“not responsible” as in single parenting is not responsible for X, Y, etc.
Amen brother! But there’s more. He continues:
Also, regarding mass immigration, be careful where you draw your lines.
The whole point of Charles Murray’s Human Acccomplishment is not just that Europeans have accomplished a lot more than other races over the past five hundred years, but that certain subgroups within western Europe proper have proven themselves to be vastly more creative than the others. Just what exactly have the Portuguese contributed to physics recently? Average IQ varies considerably among white European populations, roughly 10-12 points from the highest to the lowest, from the highest to the lowest, as does a host of other psychological dimensions such as conscientiousness, social trust, empathy, etc.
They sure do:
Average IQ across Europe
From the World Values Survey
Corruption Perceptions Index 2013, Transparency International
He continues:
There is no such thing as a singular “white” race, and there never has been — selective pressures operate a lot faster than people often imagine, and so there goes Duchesne’s crackpot Indo-European theory. Yes, human races do exist, but selection pressures are different everywhere in the world, not just on opposite sides of a continental divide. The high accomplishments of Brunelleschi, Marconi, and da Vinci are hardly reflective of the creativity of the typical lazzarone in the mezzogiorno, any more than it is possible to extrapolate directly from sharpeis to lhasa apsos.
There are rational and sensible reasons to advocate for a strict moratorium on immigration to every developed nation (not just Europe and the Anglosphere), but if you seriously want to turn back the clock at this point, why don’t we be consistent here and just kick out every single Sicilian, Irishman, or eastern Slav from the United States, considering the poorer intellectual achievement of these European populations. After all, who are they to sap the creative juices of the master race?
Thank you brother!
I don’t know if there’s just something in the air or what, but “misdreavus” managed to get out everything that has been really irking me all day long. (And believe me, I’m not the only one who felt that way, just today even!) We’ve seen “misdreavus” unload on the nutty garbage that percolates in this sphere before. One time recently was against health/obesity rubbish that is largely taken as gospel. Look, I understand that for the reasons stated above, we are going to have crazies and craziness in the HBD-sphere. And many of the more prominent individuals among these do offer quite a bit of insight, at times. Nevertheless, it often feels like I am doing double duty not just counteracting the standard PC dogma, but addressing the right-wing crazy that rails against it (who are emboldened by the wrongness of the PC liberals to believe that all of their fanciful musing is correct). This in addition to the detestable outright White supremacists in this space (or whatever you want to call yourselves – if you feel comfortable in KKK robes or wearing a Nazi uniform, you fit the mold), who, really, aren’t any more desirable to have around than, say Islamic radicals.
If the facts about heritable human differences are to be ever taken seriously, it needs to be extricated from such utter nonsense, as well as from the mean-spirited sentiment.
In any case, I feel much better now, having gotten that off my chest (it’s been bothering me for a while). Look forward to my usual fare, hitting nonsense coming from all directions, both here and on Twitter.
Also, I wanted to say thanks to all of you who have donated, it is greatly appreciated! But, I still need your help! If you’d like to donate, please do so. If you want to donate, and are having problems, please let me know, and I’ll try to make sure your donated dollars can find their way to me.
In this post, I don’t mean in the way some people might think (though it does work in that sense too), I mean in terms of longevity.
Mainstream thinkers, and some in the HBD-sphere, are fascinated and confounded by the persistent variation in health and lifespan of different peoples around the world. This has given rise to ideas like the “French Paradox,” the “Hispanic Paradox,” the “Stroke Belt,” etc. These are ongoing “mysteries” that are most confusing when you approach the situation from the paradigm that we know exactly what leads to health and long life (usually along the lines of “eating right” – whatever that happens to be at the moment – “exercise”, avoiding smoking and excessive drinking, keeping thin, etc.). These “paradoxes” arise when incongruities to this wisdom are found in the world – and there are many. Instead of doing what researchers like say, Greg Cochran and Henry Harpending, would do when you come across these mysteries – that is, at least recognize that your paradigm is faulty – what do they do? Throw their hands up in confusion and/or ignore the offending facts altogether. The latter makes it so much easier to continue as if your standard paradigm was correct.
This was recently illustrated with a rather poignant example. As many of you know, Gary Taubes recently wrote an article for the New York Times explaining why we are so ass backwards when it comes to health and nutrition. There’s not much new there. Basically he said what he, and I, have been saying for some time now – that medicine suffers from an over reliance on methodologically unsound research – especially observational studies – to derive understanding of health and the roots of human disease. While the reasons for this are somewhat understandable, fundamentally, this is no excuse if the goal is understanding human health and how to potentially help people. Much of what Taubes pointed out was affirmed in lengthy commentary by James Thompson.
Despite all this, Dr. David L. Katz, (“Director, Yale Prevention Research Center; Principal Inventor, NuVal; Editor-in-Chief, Childhood Obesity“) wrote a rebuttal to Taubes’s piece in which he dismissed the key bits of Taubes’s criticism about the methodological shortcomings of the current research, and cited the same faulty observational studies and randomized controlled trials with tiny samples to support his case for the conventional wisdom!
As disappointing as this is, this is not very surprising, unfortunately. I actually have quite a bit of experience with that, as my Twitter followers would know from my various debates with the true believers out there. (And if you’re one of them, note that I’m not trying to be mean; I am mere challenging you to think critically about your faith in the conventional wisdom). Indeed, quite timely, there was a recent article about “non-financial” conflicts of interest in academia, which noted, basically, that “people involved in a field for a long time will have established views that they will not give up easily.” Dr. Katz seems to fit the bill of this type of researcher, among numerous others. Scientists often have much more to lose than money by challenging their established view, especially if they built their career on some line of thinking.
Fortunately, you have people like me to act as a foil for this thinking.
In that, I wanted to look at those “mysteries” that befuddle mainstream researchers. One of them is the geography of life expectancy across America (from here; note that the color scales are different in each map):
These are not separated by race. But I wanted to dig into the very basic confusions that exist on this topic.
So hmmm, where have we seen these before? Oh, I know!
It is clear that something’s up in the Old South (that is, Colin Woodard‘s Greater Appalachia and the Tidewater/Deep South). By contrast, certain northern nations, particularly Yankeedom, the Left Coast, and parts of the Far West seem to live long and prosper. But why? Along the Tidewater/Deep South, it is clear that the relatively shorter lives of Blacks are involved. But Appalachia shows that it isn’t just a race issue. Some Whites live longer than other Whites. Woodard and David Hackett Fischer illustrated that intra-White regional differences are at the core of a great many things across the North American continent. One of these is health.
Let me show you something else:
This is the “Stroke Belt,” a region of America (also, interestingly, in Dixie) with an anomalously high rate of stroke deaths.
For this, while Blacks are clearly part of the equation for the heightened stroke deaths across the Deep South/Tidewater (indeed, there is some evidence that infections make Blacks more vulnerable to strokes), it isn’t just Blacks. Here are stroke deaths for Whites only (from the CDC):
Once again the usual suspects crop up: Greater Appalachia, the Tidewater, and the Deep South. However, stroke risk also appears elevated on the Left Coast as well.
But note where life expectancy is particularly good and stroke risk is particularly low: El Norte. Which brings me to the “Hispanic Paradox.”
Anatoly Karlin recently commented on this. That is, Hispanics tend to live longer than you would “expect” given their socioeconomic status and conditions like obesity and the classic “health markers” and such:
Now you know I’ve had a few things to say about that (for which those who are familiar with this might know where I’m going with this).
Henry Harpending once posted on the apparent longevity of U.S. Hispanics. Lets look at something else:
These are maps of life expectancy at birth across Europe, in 2004 (males top, females bottom, from here). As we’ve seen before, there is a distinct southwest to northeast gradient in life expectancy, following the rate of cardiovascular mortality on the continent (of course, we know, thanks to NBC’s Dr. Nancy Snyderman, that this is due to the Slavs’ poor diets).
These maps break it down further, so we can see the regional differences (from here and here, respectively):
As we can see, some countries have significant regional variation. Oddly enough, it is all the usual suspects (the U.K., France, Germany, and to a lesser extent, Spain and Portugal). A key part of the “Hispanic paradox” may be the somewhat long-lived Iberian component.
Of course, this would predict that life expectancies in Latin America would be on the high side. Are they?
This is life expectancy across the world, 2003 (from the WHO). Life expectancy is highish in Latin America by global standards. The connection is especially evident in the more Iberian countries (e.g., Chile, Uruguay) vs. the more Indigenous ones (e.g., Bolivia). I suppose if I were more inclined, I could look up life expectancy with homicide and accidents removed (which is likely suppressing these numbers here).
Looking at life expectancies across the U.S., one can see that the life expectancy of each region is related to the predominant ethnic group that resides in them. Most striking is Greater Appalachia. As with the Celtic fringes of Britain, life expectancy is notably lower among the American Scotch-Irish.
That’s not the only problem that seems to plague the Borderlanders. They seem to be particularly prone to addiction, as seen by smoking:
Alcoholism, at least by remaining dry counties (blue = wet; red = dry; yellow = mix):
Much can be traced to Americans’ cousins across the Atlantic.
Indeed, as we saw in my earlier post A Fat World – With a Fat Secret?, obesity clusters by ethnicity. Americans are not anomalously fat by global standards, at least not when you consider race and the other Anglo nations – contrary to what the popular press would lead you to believe.
Indeed, the clustering of health and physiological features like fatness by ethnicity should not be surprising when you consider the heritable component to these things. But since conventional wisdom, even in the HBD-sphere, likes to blame health outcomes on lifestyle-only, some may be shocked by these patterns.
Now, while my discussion on the matter may give the impression that I believe diet and lifestyle plays no role in health outcomes, the reality is that this is not the case. I will concede that likely it does have some effect. It’s just that the evidence for lifestyle being the panacea it is commonly believed to be is lacking. One possible example of the role of lifestyle is the island of Okinawa. Okinawans, famous for their longevity, have been taking a hit lately, apparently due to the adoption of a Western diet. It is worth noting that some groups, especially those adapted to highly specialized diets, might be adversely affected by the shift to “Western” diets. This doesn’t appear to be a major problem for Japan in general (but may be true in China). Further research is needed.
And this brings me to my final point, and why the diet and lifestyle issue has been a real bugger for me: as with HBD-denial in general, the thing that pisses me off most is not the implications of the denial, which are rather significant to be sure. It is that it holds back the science. Imagine how far we could have gotten by now if we didn’t go the route that Gary Taubes laments (reliance on observational studies) and particularly, didn’t discount heredity and the fact that people are not interchangeable. I’d imagine we could have gotten a great deal further. Cochran and Harpending both lament the broad uselessness of both most scientists and modern journalists. Indeed, much of what I have discussed in this blog post is pretty low-hanging fruit, and could easily have been examined if someone bothered to look. Oh well, for now, at least, that’s why people like me are here.
Please see my earlier post about the new funding drive I’m running. Fortunately I have been able to make do with access to some of the computers I have to make this post. But I still need your help. Please, if you can and would like to help, donate. Thank you!
So it seems my blogging will be slower than I anticipated, because now I’ve hit a snag in the form of computer failure. I won’t be able to put out comprehensive blog posts for a bit. Well, actually, this is only one of many hardware problems I have at the moment, but I won’t burden you with all my woeful details… 🙂
So as you would imagine, with a new child, finances to fix the problem aren’t easy to come by. So things will be slow around here. But, in the mean time, you can still enjoy my bits of insight on Twitter and my commentary across the blogosphere.
Also, you can amuse yourself by reading my older posts. There’s plenty of good stuff there, see:
100 Blog Posts – A Reflection on HBD Blogging And What Lies Ahead
My monthly archives, especially these two busy months for me:
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As always, I appreciate any support you can give me!
In the wake of the recent snow storm in the Deep South, The Atlantic recently released an article with a map made by Reddit user Alexandr Trubetskoy with the typical amount of snowfall it takes to cancel schools in the different counties across America. Since I couldn’t resist, I thought I’d put Colin Woodard’s American Nations boundaries over that map. Here’s the result:
Yes, the American nations are visible even in snow cancellation policy. Now, as noted in The Atlantic article, the situation on the ground is a bit more nuanced than this map represents. Nonetheless, the relationship is striking.
This map is heavily indicative of climate of these respective counties. The snow policy is itself a response to the amount of snow these areas typically receive, as seen here:
If we closed the schools here in Maine every time it snowed, they’d be closed for a third to half the semester. And of course, the more snow you typically receive, the more you have to adopt contingency measures for dealing with winter weather. Many Mainers were quite amazed at the chaos that ensued in the South when they received (as my wife put it), “a dusting.”
But that the American nations would follow climatic lines isn’t surprising. Colonial expansion to the interior of the continent often flowed nearly due west, to places with similar weather.
It simply made sense, whenever possible, to expand into areas where you could simply copy the way of life with which you were adapted, instead of having to start fresh. This is reflected today in the snow cancellation policy, as it is in many other things.
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