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 in 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.
“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:
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.
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:
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.
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:
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:
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.
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.
The theme for this post is a cue from the original Robocop, something which I feel fits the tone of this post…
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):
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).
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):
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:
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.