Heritability & Inheritance, Genetics & Epigenetics, Etc

There is so much misinformation and misunderstanding about genetics, inheritance and heritability; also the emerging field of epigenetics. Few discussions online about race, IQ, etc seem worthy of taking seriously. I admit that I don’t understand much about this field of science, but I at least acknowledge its complexity. Some others, however, wish to assert more certainty than the scientific evidence strictly allows.

I have little desire to try to summarize, much less analyze, all of the complexities, even if I did comprehend it well enough to do so. Besides, that is more than is possible in a single blog post. Instead, I’ll offer more than a few helpful resources. Below are some articles and, following that, some passages from books I’ve been reading. If you wish to actually understand these issues or at least not appear absolutely stupid in a discussion, reading these sources might be a good place to start in order to give yourself at least a basic grasp of the diverse research and the key distinctions to keep in mind.

I’ve been slowly working my way through a bunch of dense books (a few of them are found below). I’m trying my best to make sense of this difficult area of knowledge. My only purpose in spending my time in this fashion is to create a groundwork for discussion of the more social and cultural issues that I’m interested in. I want to be able to articulate what the data does and doesn’t show us, maybe even according to present limits of science what it can and can’t show us. I want to get past all the ideological biases and assumptions, on all sides, so as to get to the heart of the matter.

My hope is, in my own small way, to further discussion. To do so, I need to inform myself and in the process maybe others will be better informed as well. The following is some small part of the results of my ongoing studies. It is information to be considered.

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Genetic vs. heritable trait
By Razib Khan
Discover Magazine

Rethinking The Genetic Theory Of Inheritance: Heritability May Not Be Limited To DNA
Science Daily

Missing Heritability — Or Whole-Organism Inheritance?
Stephen L. Talbott
The Nature Institute

Rethinking inheritance
Cell Press Discussions

We Still Don’t Know Why We Look Like Our Parents
Genetics? Sure, but it’s not that simple.
By Michael White
Pacific Standard Magazine

Schizophrenia is (arguably*) 80% heritable; it is not 80% genetic
Manchester Psychiatry Society Blog

No Genes for Intelligence
Institute of Science in Society

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What’s the Use of Race?: Modern Governance and the Biology of Difference
By Ian Whitmarsh and David S. Jones
pp. 52-3

As critics stress (McCabe and McCabe 2006), the relationship between genotype and phenotype is complex. It is well understood only in exceptional cases, such as single gene diseases like Huntington’s disease or cystic fibrosis, where the presence of a specific, single, changed gene predicts the disease, virtually without exception. Historically, scientists assumed that more conditions would mirror the single gene model and that scientific advances would proceed by identifying a limited set of disease genes with treatments targeted at the associated phenotypes. But these assumptions are increasingly being proved wrong. Instead, researchers are discovering complex, highly contingent relationships between genotype and phenotype that challenge ready explanation. Some are associated with epigenetic events, which are heritable changes in phenotype or gene expression that result from influences external to changes in the underlying DNA (Riddihough and Pennisi 2001). Others remain unexplained, and in many fields, understanding of the genotype-phenotype relationship seems to recede, rather than advance, despite intensive study (Gaedigk et al. 2005; McCabe and McCabe 2006).

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What Is Intelligence?
By James Flynn
pp. 39-40

In other words, genetic advantages that may have been quite modest at birth have a huge effect on eventual basketball skills by getting matched with better environments – and genes thereby get credit for the potency of powerful environmental factors, such as more practice, team play, professional coaching. It is not difficult to apply the analogy to IQ. One child is born with a slightly better brain than another. Which of them will tend to like school, be encouraged, start haunting the library, get into top-stream classes, and attend university? And if that child has a separated identical twin that has much the same academic history, what will account for their similar adult IQs? Not identical genes alone – the ability of those identical genes to co-opt environments of similar quality will be the missing piece of the puzzle.

Note that genes have profited from seizing control of a powerful instrument that multiplies causal potency, namely, feedback loops that operate between performance and its environment. A gene-caused performance advantage causes a more-homework-done environment, the latter magnifies the academic performance advantage, which upgrades the environment further by entry into a top stream, which magnifies the performance advantage once again, which gets access to a good university environment. Since these feedback loops so much influence the fate of individuals throughout their life histories, the Dickens/Flynn model calls them “individual multipliers.”

Understanding how genes gain dominance over environment in kinship studies provides the key to how environment emerges with huge potency between generations. There must be persistent environmental factors that bridge the generations; and those factors must seize control of a powerful instrument that multiplies their causal potency.

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Ungifted: Intelligence Redefined
By Scott Barry Kaufman
pp. 6-9

In 1990 the behavioral geneticist Thomas J. Bouchard Jr. and his colleagues at the University of Minnesota published a striking finding: about 70 percent of the differences in IQ found among twins and triplets living apart were associated with genetic variation. 8 What’s more, the identical twins (whose genes were assumed to be 100 percent identical * ) were remarkably similar to identical twins reared together on various measures of personality, occupational and leisure-time interests, and social attitudes, despite spending most of their lives apart.

This study, and the hundreds of twin and adoption studies that have been conducted since then, have painted a consistent picture: genetic variation matters. 9 The studies say nothing about how they matter, or which genes matter, but they show quite convincingly that biological variation does matter. Genes vary within any group of people (even among the inhabitants of middle-class Western society), and this variation contributes to variations in these people’s behaviors. The twin findings shouldn’t be understated; it counters many a prevailing belief that we are born into this world as blank slates, completely at the mercy of external forces. 10

The most important lesson researchers have learned from over twenty-five years’ worth of twin studies is that virtually every single psychological trait you can measure— including IQ, personality, artistic ability, mathematical ability, musical ability, writing, humor styles, creative dancing, sports, happiness, persistence, marital status, television viewing, female orgasm rates, aggression, empathy, altruism, leadership, risk taking, novelty seeking, political preferences, television viewing, and even rates of Australian teens talking on their cell phones— has a heritable basis. * Because our psychological characteristics reflect the physical structures of our brains and because our genes contribute to those physical structures, it is unlikely that there are any psychological characteristics that are completely unaffected by our DNA. 11

Unfortunately there is frequent confusion about the meaning of heritability. The most frequent misunderstanding is the purpose of twin studies. Heritability estimates are about understanding sources of similarities and differences in traits between members of a particular population. The results apply only to that population. The purpose is not to determine how much any particular individual’s traits are due to his or her genes or his or her environment. Behavioral geneticists are well aware that all of our traits develop through a combination of both nature and nurture. Heritability estimates are about explaining differences among people, not explaining individual development. The question on the table for them is this: In a particular population of individuals, what factors make those individuals the same as each other, and which factors make them different?

Therefore, twin studies aren’t designed to investigate human development. In recent years developmental psychologists, including L. Todd Rose, Kurt Fischer, Peter Molenaar, and Cynthia Campbell, have been developing exciting new techniques to study intraindividual variation. 12 Intraindividual variation focuses on a single person and looks at how an integrated dynamic system of behavioral, emotional, cognitive, and other psychological processes change across time and situations. New intraindividual techniques allow researchers to focus on a single twin pair and see how nature and nurture interact in nonlinear ways to explain both their similarities and their differences. 13 Both levels of analysis— twin studies and developmental analysis— are informative, but the results from the one do not apply to the other. 14

Many people also confuse heritability with immutability. They hear the word “heritable” and immediately think of “genes,” which then conjures up pictures of a fixed trait that can’t be altered by external forces. In contrast, many people hear the word “environment” and breathe a sigh of relief, thinking the trait is easily modifiable. This requires quite a strong faith in social engineering!

Just because a trait is heritable (and virtually all of our psychological traits are heritable) doesn’t necessarily mean that the trait is fixed or can’t be developed. Virtually all of our traits are substantially genetically influenced and are influenced by environmental conditions. Even though television viewing has a heritable basis, 15 most people don’t think of the activity as being outside our personal control. Indeed, parents frequently control (or try to control) the length of time their children spend sitting in front of the tube.

Another source of confusion is the role of parenting in the development of traits. A common finding in twin studies is that the environments experienced by twins (or any two siblings) do little to create differences in intelligence and personality as adults. In other words, the heritability of traits tends to increase as one ages and escapes the influence of parents. 16 Judith Rich Harris showed that peers exert a greater influence in creating differences in personality among adolescents than parents. 17 But do these findings mean that parents cannot effectively help their child develop their unique traits? Absolutely not. That’s like saying that water has no influence on a fish’s development because all fish live in water. A nurturing family environment is a necessity to help the child flourish, just as a fish needs water to swim and survive.

Just because a variable doesn’t vary doesn’t mean it has no causal impact on a particular outcome. Genes could “account for” 100 percent of the variability in a trait in a particular twin study, but this does not mean that environmental factors, including parental quality, are therefore unimportant in the development of the trait. Instead it turns out that parenting matters in a way that is different from what was originally assumed: Parents matter to the extent that they affect the expression of genes. Parents can exert important influence in the child’s development by nurturing productive interests and helping the child channel destructive inclinations into more productive outlets.

The importance of parenting becomes more salient when we look at a wider range of environments. Only a few of the twins in Bouchard’s original study were reared in real poverty or were raised by illiterate parents, and none were mentally disabled. This matters. Consider a recent study by Eric Turkheimer and colleagues. They looked at 750 pairs of American twins who were given a test of mental ability when they were 10 months old and again when they were 2 years. 18 When looking at the group of kids aged just 10 months, the home environment appeared to be the key variable across different levels of socioeconomic status. The story changed considerably as the children got a bit older and differences in education became more pronounced. For the 2-year-olds living in poorer households, the home environment mattered the most, accounting for about 80 percent of the variation in mental ability. For these kids, genetics played little role in explaining differences in cognitive ability. In wealthy households, on the other hand, genetics explained more of the differences in performance, accounting for nearly 50 percent of all the variation in mental ability.

Prominent behavioral geneticists, including Bouchard, eventually realized that it was time to move on from simply calculating heritability estimates . In a 2009 paper entitled “Beyond Heritability,” researchers Wendy Johnson, Eric Turkheimer, Irving I. Gottesman, and Bouchard concluded that “given that genetic influences are routinely involved in behavior,” “little can be gleaned from any particular heritability estimate and there is little need for further twin studies investigating the presence and magnitude of genetic influences on behavior.” 19

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The Mismeasure of Man (Revised & Expanded)
By Stephen Jay Gould
Kindle Locations 463-486

Errors of reductionism and biodeterminism take over in such silly statements as “Intelligence is 60 percent genetic and 40 percent environmental.” A 60 percent (or whatever) “heritability” for intelligence means no such thing. We shall not get this issue straight until we realize that the “interactionism” we all accept does not permit such statements as “Trait x is 29 percent environmental and 71 percent genetic.” When causative factors (more than two, by the way) interact so complexly, and throughout growth, to produce an intricate adult being, we cannot , in principle, parse that being’s behavior into quantitative percentages of remote root causes. The adult being is an emergent entity who must be understood at his own level and in his own totality. The truly salient issues are malleability and flexibility, not fallacious parsing by percentages. A trait may be 90 percent heritable, yet entirely malleable. A twenty-dollar pair of eyeglasses from the local pharmacy may fully correct a defect of vision that is 100 percent heritable. A “60 percent ” biodeterminist is not a subtle interactionist , but a determinist on the “little bit pregnant” model.

Thus, for example, Mr. Murray, in high dudgeon about my review of The Bell Curve (reprinted here as the first essay in the concluding section), writes in the Wall Street Journal ( December 2, 1994), excoriating my supposed unfairness to him:

Gould goes on to say that “Herrnstein and Murray violate fairness by converting a complex case that can yield only agnosticism into a biased brief for permanent and heritable differences.” Now compare Mr. Gould’s words with what Richard Herrnstein and I wrote in the crucial paragraph summarizing our views on genes and race: “If the reader is now convinced that either the genetic or environmental explanations have won out to the exclusion of the other, we have not done a sufficiently good job of presenting one side or the other. It seems highly likely to us that both genes and the environment have something to do with racial differences. What might the mix be?”

Don’t you get it yet, Mr. Murray? I did not state that you attribute all difference to genetics— no person with an iota of knowledge would say such a foolish thing. My quoted line does not so charge you; my sentence states accurately that you advocate “permanent and heritable differences”— not that you attribute all disparity to genetics. Your own defense shows that you don’t grasp the major point. Your statement still portrays the issue as a battle of two sides, with exclusive victory potentially available to one. No one believes such a thing; everyone accepts interaction. You then portray yourself as a brave apostle of modernity and scholarly caution for proclaiming it “highly likely … that both genes and the environment have something to do with racial differences.” You have only stated a truism entirely outside the real issue. When you make the proper distinction between heritability and flexibility of behavioral expression, then we might have a real debate beyond the rhetoric of phrasing.

Kindle Locations 2937-2939

Within- and between-group heredity are not tied by rising degrees of probability as heritability increases within groups and differences enlarge between them. The two phenomena are simply separate . Few arguments are more dangerous than the ones that “feel” right but can’t be justified.

Kindle Locations 6022-6041

The central fallacy in using the substantial heritability of w.thin-group IQ (among whites, for example) as an explanation for average differences between groups (whites vs. blacks, for example) is now well known and acknowledged by all, including Herrnstein and Murray, but deserves a restatement by example. Take a trait far more heritable than anyone has ever claimed for IQ, but politically uncontroversial— body height. Suppose that I measure adult male height in a poor Indian village beset with pervasive nutritional deprivation. Suppose the average height of adult males is 5 feet 6 inches, well below the current American mean of about 5 feet 9 inches. Heritability within the village will be high— meaning that tall fathers (they may average 5 feet 8 inches) tend to have tall sons , while short fathers (5 feet 4 inches on average) tend to have short sons. But high heritability within the village does not mean that better nutrition might not raise average height to 5 feet 10 inches (above the American mean) in a few generations. Similarly the well-documented 15-point average difference in IQ between blacks and whites in America, with substantial heritability of IQ in family lines within each group, permits no conclusion that truly equal opportunity might not raise the black average to equal or surpass the white mean.

Since Herrnstein and Murray know and acknowledge this critique, they must construct an admittedly circumstantial case for attributing most of the black-white mean difference to irrevocable genetics— while properly stressing that the average difference doesn’t help at all in judging any particular person because so many individual blacks score above the white mean in IQ. Quite apart from the rhetorical dubriety of this old ploy in a shopworn genre—“ some-of-my-best-friends-are-group-x”—Herrnstein and Murray violate fairness by converting a complex case that can only yield agnosticism into a biased brief for permanent and heritable difference. They impose this spin by turning every straw on their side into an oak, while mentioning but downplaying the strong circumstantial case for substantial malleability and little average genetic difference (impressive IQ gains for poor black children adopted into affluent and intellectual homes; average IQ increases in some nations since World War II equal to the entire 15-point difference now separating blacks and whites in America; failure to find any cognitive differences between two cohorts of children born out of wedlock to German women, and raised in Germany as Germans, but fathered by black and white American soldiers).

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The Emperor’s New Clothes: Biological Theories of Race at the Millennium
Joseph L. Graves Jr.
Kindle Locations 2115-2146

Such inconsistencies also demonstrate that the psychometricians have only an amateurish grasp of evolutionary genetics. Numerous errors flow from this lack of scientific perspective. The vast majority of Herrnstein and Murray’s evidence is based on phenotypic information; that is, the reputed difference between races is based on some indirect measure of cognitive function, usually a standardized test. The reliance on such tests is made worse by the fact that they have not been conclusively shown to properly measure intellectual function. From these tests, psychometricians infer an underlying genetic difference, despite the fact that standard quantitative genetic protocols are premised on the extensively corroborated demonstration that procedures such as theirs are scientifically invalid. The flaws in their research program are best illustrated in their obsession with the false association between “group heritability” and the necessity of racial differences in IQ. They presume they can show that IQ is inherited genetically and that there must be substantial genetically based differences between the races. Their focus on genetic predestination of intellectual ability is thus their rationale for supporting the status quo because, in their rather limited view, genes cannot be easily altered.

Heritability in the Psychometric Worldview

Much of the argument concerning racial differences in intelligence has focused on an inappropriate assumption, that is, the heritability of IQ. Throughout the debate on race and intelligence, the methodologies used to establish heritability have been fraught with error and fraud. Psychometricians often ignore basic difficulties in estimating quantitative genetic formulas for variation. The fact that IQ test scores have a continuous distribution indicates that whatever cognitive functions are related to these tests must be influenced by many genetic and environmental factors. The formal expression for heritability in the broad sense is simply the ratio of variance in the character due to genetic sources, over all sources of variance. Direct estimates of heritability in laboratory studies can be tedious. They require rigorous control of confounding environmental factors and careful measurements of the phenotype in question.

Consider the equation for VP, the variance in the phenotype:

VP = Vg + Ve + Vg X e + Cov(g,e) + Verroo

where Vg = variance of genetic origin, Ve = variance of environmental origin, Vg X e = variance due to gene X environment interaction, Cov(g,e) = the covariance of genes and environment, and Verror = variance due to errors in measurement. This equation illustrates that one cannot infer that a phenotypic difference between two groups automatically indicates a genetic difference. Under laboratory conditions we can control the environment such that we can eliminate the third and fourth terms of the equation. For example, if we measure the longevity of fruit flies from two different populations and hold all environmental conditions the same for both groups, then we can safely assume that the third and fourth terms are close to zero. This leaves

VP =Vg + Ve + Verror’

If we have carefully measured the longevity phenotype, then we can assume that the difference between the two populations is indeed due to genetic sources. However, there is an additional caveat: before we can make these measurements we must rear the flies under identical conditions for at least two generations because complex phenotypes are strongly influenced by maternal environmental effects. The environmental conditions experienced during development can influence the expression of genes in the adult. It should be clear that none of the rigorous controls that are required to identify genetic effects in the laboratory exist under the conditions in which attempts to measure human IQ have been made.

Psychometricians emphasize the heritability of intelligence. But the particular estimate of the heritability of intelligence, however defined, has little to do with the question of cognitive differences between races because the estimates used to calculate the heritability of intelligence result from studies of close relatives. We already know that most of the genetic variability in the human species is at the level of individuals or families. But family-level variation does not therefore translate directly into racial variation. Data from an experiment in my laboratory examining the effect of a known genetic substitution on the complex trait of longevity revealed significant variation in families within populations but no significant variation between the populations. That is, both populations had family genetic backgrounds that responded differentially to the genetic substitution when measured under rigorously controlled environmental conditions. This is another way of saying that if genes do influence intelligence, then we should expect that all races will have families that run the range of the genetic variability for intelligence. Thus, given the large genetic overlap of human populations, our expectation should be that there is no significant racial difference in intelligence or other behavioral traits.

To this prediction the racists will howl, How then do you explain the persistent IQ differential reported by twentieth-century studies? The answer is elementary; let us look at the conditions under which the tests were given. Do they really adhere to the requirements of a valid test of genetic differentiation? Absolutely not. The problems of the psychometric program do not improve when it attempts to look at specific “genetic” systems reputedly associated with intelligence. After all, Arthur Jensen even admitted that there should be many genes that impact the expression of intelligence, precisely because it is a polygenic trait. It is significant that the psychometricians have been unable to properly define the physiological traits that are purportedly responsible for intelligence and that are differentiated among the racial groups. This lack of precision makes attempts at localizing the genes involved very difficult.

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The Bell Curve Wars: Race, Intelligence, and the Future of America
By Steven Fraser
Kindle Locations 163-174

Herrnstein and Murray’s second claim, the lightning rod for most commentary, extends the argument for innate cognitive stratification to a claim that racial differences in IQ are mostly determined by genetic causes-small difference for Asian superiority over Caucasian, but large for Caucasians over people of African descent. This argument is as old as the study of race, and is most surely fallacious. The last generation’s discussion centered on Arthur Jensen’s 1980 book Bias in Mental Testing (far more elaborate and varied than anything presented in The Bell Curve, and therefore still a better source for grasping the argument and its problems), and on the cranky advocacy of William Shockley, a Nobel Prize-winning physicist. The central fallacy in using the substantial heritability of within-group IQ (among whites, for example) as an explanation of average differences between groups (whites versus blacks, for example) is now well known and acknowledged by all, including Herrnstein and Murray, but deserves a restatement by example. Take a trait that is far more heritable than anyone has ever claimed IQ to be but is politically uncontroversial-body height. Suppose that I measured the heights of adult males in a poor Indian village beset with nutritional deprivation, and suppose the average height of adult males is five feet six inches. Heritability within the village is high, which is to say that tall fathers (they may average five feet eight inches) tend to have tall sons, while short fathers (five feet four inches on average) tend to have short sons. But this high heritability within the village does not mean that better nutrition might not raise average height to five feet ten inches in a few generations. Similarly, the well-documented fifteen-point average difference in IQ between blacks and whites in America, with substantial heritability of IQ in family lines within each group, permits no automatic conclusion that truly equal opportunity might not raise the black average enough to equal or surpass the white mean.

Kindle Locations 2281-2307

Ironically, one of the best arguments against the hereditarian approach comes from the genetics of heredity itself.

Heritability (h2), it will be recalled, is technically defined as the percentage of total phenotypic variance in a given trait which is explained by the genes in question, for a given population. More technically, it is the ratio of the additive genetic variance to the phenotypic variance of the trait or character being considered: h2= Vg/Vp. The fact that it is only the additive variance (Va) which enters the equation must be emphasized, since an important additional fact usually goes unmentioned, especially by psychologists, in discussions of heredity. This is the fact that total genetic variance actually contains two other elements, namely, dominance variance (Vd) and epistatic or genetic interaction variance (Vi). Hence complete genetic variance is properly given by the additive equation: Vg = Va + Vd + Vi. Further, taking environment (e) into account, total phenotypic variance on a given trait is Vp = Vg + Ve.

Now, recall that, throughout The Bell Curve, and indeed among all hereditarian psychologists, it is claimed that intelligence, as measured by IQ tests, is highly hereditary: ranging between .40 and .80, and taken to be .60 by Herrnstein and Murray. If we return to the equation for heredity which is commonly employed-and the one used throughout The Bell Curve-(h2= Vg/Vp) in the light of one well established principle of genetic selection, we are immediately faced with what Vale calls a “nice irony.” The selection principle in question is the fact that any trait which has been under strong selection for a long evolutionary period will demonstrate very little additive genetic variance and should consist mainly of dominance and possibly epistatic variance, the reason being that almost all the additive genetic variance-which is the only component of the three elements of total genetic variance that responds to evolutionary selection-will have been “used up,” so to speak. This being so, the hereditarians are faced with an embarrassing, because inexplicable, dilemma. To quote Vale:

It is true of fitness characters that the proportion of additive genetic variance is small. It is therefore noteworthy that not only the total genetic component of variance (heredity in the broad sense or the degree of genetic determination) of IQ has been found to be so large, but that the proportion of additive variance within that component has been found to contribute the most to it…. The question is: If IQ is fitness character, why should the additive variance be anywhere near .71?

Or .60 or .40 or for that matter anywhere other than hovering close to zero, which is where one expects to find the additive genetic variance of a trait that, as the hereditarian psychologists claim, and we fully agree, has been highly selected as an essential factor in the survival and fitness of the human species to its environment.

The problem which Herrnstein, Jensen, and all hereditarian psychologists face then, from the discipline on which they have so heavily drawn, is that IQ scores are too hereditary if they are to sustain the claim that these tests have any significance beyond the test center and classroom. Whatever it is that IQ tests are measuring, whatever it is that g is-whether it be some Platonic ideal, or g for ghost, a pun which Ryle might not have intended when he dismissed the whole thing in his Concept of Mind as “the ghost of the machine”-it could have nothing whatever to do with those vitally important behavioral qualities that meaningfully account for our survival in both broad evolutionary and narrower sociological terms.

I return, then, to my more familiar sociological terrain with this understanding of the problem. Intelligence is not an essence but a process, not some operationally inferred static entity, indicated by IQ tests-and the much beloved analogies with the discovery of gravity and electricity are as pretentious and silly as the tautology that intelligence is whatever it is that IQ tests are testing’-but that mode of thinking, symbolizing, acting, and interacting which, in their totality, facilitates survival in, and/or mastery of, its environment by an individual or group. It is acknowledged that cognitive functioning is central to this behavioral configuration, and further, that genetic factors are important in its determination-that, indeed, intelligence was a major factor in our evolution as a species-but that there is absolutely no way in which we can meaningfully separate genetic and environmental effects, and that, given the impossibility of conducting experiments on human populations, it is practically impossible, theoretically misguided, sociologically reprehensible, and morally obtuse to attempt to separate or even talk about the two as distinct processes.

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Race and the Genetic Revolution: Science, Myth, and Culture
“Intelligence, Race, and Genetics”
By Robert J. Sternberg, Elena L Grigorenko, Kenneth K. Kidd, and Steven E. Stemler
pp. 216-220

Most recently, Deary et al. found that “there is still almost no replicated evidence concerning the individual genes, which have variants that contribute to intelligence differences.”89 Of course, the future may bring conclusive identifications: we just do not know yet.

As a result, virtually all attempts to study genes related to intelligence have been indirect, through studies of heritability. But heritability is itself a troubled concept. Are differences in intelligence between so-called races heritable? The question is difficult to answer in part because it is difficult even to say what can be concluded from the heritability statistic commonly used. Consider some facts about heritability.90

What Heritability Tells Us

Heritability (also referred to as h2) is the ratio of genetic variation to total variation in an attribute within a population. Thus, the coefficient of heritability tells us nothing about sources of between-population variation. Moreover, the coefficient of heritability does not tell us the proportion of a trait that is genetic in absolute terms, but rather, the proportion of variation in a trait that is attributable to genetic variation within a specific population.

Trait variation in a population is referred to as phenotypic variation, whereas genetic variation in a population is referred to as genotypic variation. Thus, heritability is a ratio of genotypic variation to phenotypic variation. Heritability has a complementary concept, that of environmentality. Environmentality is a ratio of environmental variation to phenotypical variation. Note that both heritability and environmentality apply to populations, not to individuals. There is no way of estimating heritability for an individual, nor is the concept meaningful for individuals. Consider a trait that has a heritability statistic equaling 70 percent; it is nonsense to say that the development of the trait in an individual is 70 percent genetic.

Heritability is typically expressed on a 0 to 1 scale, with a value of 0 indicating no heritability whatsoever (i.e., no genetic variation in the trait) and a value of 1 indicating complete heritability (i.e., only genetic variation in the trait). Heritability and environmentality add to unity (assuming that the error variance related to measurement of the trait is blended into the environmental component). Heritability tells us the proportion of individual-difference variation in an attribute that appears to be attributable to genetic differences (variation) within a population. Thus, if IQ has a heritability of .50 within a certain population, then 50 percent of the variation in scores on the attribute within that population is due (in theory) to genetic influences. This statement is completely different from the statement that 50 percent of the attribute is inherited.

An important implication of these facts is that heritability is not tantamount to genetic influence. An attribute could be highly genetically influenced and have little or no heritability. The reason is that heritability depends on the existence of individual differences. If there are no individual differences, there is no heritability (because there is a 0 in the denominator of the ratio of genetic to total trait variation in a given population). For example, being born with two eyes is 100 percent under genetic control (except in the exceedingly rare case of severe dismorphologies, with which we will not deal here). Regardless of the environment into which one is born, a human being will have two eyes. But it is not meaningful to speak of the heritability of having two eyes, because there are no individual differences. Heritability is not 1: it is meaningless (because there is a 0 in the denominator of the ratio) and cannot be sensibly calculated.

Consider a second complementary example, occupational status. It has a statistically significant heritability coefficient associated with it,91 but certainly it is not under direct genetic control. Clearly there is no gene or set of genes for occupational status. How could it be heritable, then? Heredity can affect certain factors that in turn lead people to occupations of higher or lower status. Thus, if things like intelligence, personality, and interpersonal attractiveness are under some degree of genetic control, then they may lead in turn to differences in occupational status. The effects of genes are at best indirect.92 Other attributes, such as divorce, may ran in families, that is, show familiality, but again, they are not under direct genetic control; in fact, the familiality may be because they are culturally “inherited.”

Heritability Can Vary Within a Given Population

Heritability is not a fixed value for a given attribute. Although we may read about “the heritability of IQ,”93 there really is no single fixed value that represents any true, constant value for the heritability of IQ or anything else, as Herrnstein and Murray and most others in the field recognize.94 Heritability depends on many factors, but the most important one is the range of environments. Because heritability represents a proportion of variation, its value will depend on the amount of variation. As Herrnstein pointed out, if there were no variation in environments, heritability would be perfect, because there would be no other source of variation.95 If there is wide variation in environments, however, heritability is likely to decrease.

When one speaks of heritability, one needs to remember that genes always operate within environment contexts. All genetic effects occur within a reaction range, so that, inevitably, environment will be able to have differential effects on the same genetic structure. The reaction range is the range of phenotypes (observable effects of genes) that a given genotype (latent structure of genes) for any particular attribute can produce, given the interaction of environment with that genotype. For example, genotype sets a reaction range for the possible heights a person can attain, but childhood nutrition, diseases, and many other factors affect the adult height realized. Moreover, if different genotypes react differently to the environmental variation, heritability will show differences depending on the mean and variance in relevant environments.96 Thus, the statistic is not a fixed value. There are no pure genetic effects on behavior, as would be shown dramatically if a child were raised in a small closet with no stimulation. Genes express themselves through covariation and interaction with the environment, as discussed further later.

Heritability and Modifiability

Because the value of the heritability statistic is relevant only to existing circumstances, it does not and cannot address a trait’s modifiability. A trait could have zero, moderate, or even total heritability and, in any of these conditions, be not at all, partially, or fully modifiable. The heritability statistic deals with correlations, whereas modifiability deals with mean effects. Correlations, however, are independent of score levels. For example, adding a constant to a set of scores will not affect the correlation of that set with another set of scores. Consider height as an example of the limitation of the heritability statistic in addressing modifiability. Height is highly heritable, with a heritability of over .90. Yet height also is highly modifiable, as shown by the fact that average heights have risen dramatically throughout the past several generations.

As an even more extreme example, consider phenylketonuria (PKU). PKU is a genetically determined, recessive condition that arises due to a mutation (or, rather, a number of various rare mutations resulting in similar functional damages to the coded protein, see below) in a single gene, the PAH gene, on chromosome 12 (with a heritability of 1), and yet its effects are highly modifiable. Feeding an infant with PKU a diet free of phenylalanine prevents the mental retardation that otherwise would become manifest. Note also that a type of intellectual disability that once incorrectly was thought to be purely genetic is not. Rather, the intellectual disability associated with PKU is the result of the interaction with an environment (a “normal” diet) in which the infant ingests phenylalanine. Take away the phenylalanine and you reduce level of, or, in optimal cases, eliminate intellectual disability. Note that the genetic endowment does not change: the infant still has a mutant gene causing phenylketonuria. What changes is the manifestation of its associated symptoms in the environment. Similarly, with intelligence or any other trait, we cannot change (at least with our knowledge today) the genetic structure underlying manifestations of intelligence, but we can change those manifestations, or expressions of genes in the environment. Thus, knowing the heritability of a trait does not tell us anything about its modifiability.

* * * * *

The Genius in All of Us: New Insights into Genetics, Talent, and IQ
By David Shenk
Kindle Locations 1003-1031

But the nature of that genetic influence is easily— and perilously— misinterpreted. If we are to take the word “heritability” at face value, genetic influence is a powerful direct force that leaves individuals rather little wiggle room. Through the lens of this word, twin studies reveal that intelligence is 60 percent “heritable,” which implies that 60 percent of each person’s intelligence comes preset from genes while the remaining 40 percent gets shaped by the environment. This appears to prove that our genes control much of our intelligence; there’s no escaping it.

In fact, that’s not what these studies are saying at all.

Instead, twin studies report, on average, a statistically detectable genetic influence of 60 percent. Some studies report more, some a lot less . In 2003, examining only poor families, University of Virginia psychologist Eric Turkheimer found that intelligence was not 60 percent heritable, nor 40 percent, nor 20 percent, but near 0 percent —demonstrating once and for all that there is no set portion of genetic influence on intelligence. “These findings,” wrote Turkheimer , “suggest that a model of [genes plus environment] is too simple for the dynamic interaction of genes and real-world environments during development.”

How could the number vary so much from group to group? This is how statistics work. Every group is different; every heritability study is a snapshot from a specific time and place, and reflects only the limited data being measured (and how it is measured).

More important, though, is that all of these numbers pertain only to groups— not to individuals. Heritability, explains author Matt Ridley , “is a population average, meaningless for any individual person : you cannot say that Hermia has more heritable intelligence than Helena. When somebody says that heritability of height is 90 percent, he does not and cannot mean that 90 percent of my inches come from genes and 10 percent from my food. He means that variation in a particular sample is attributable to 90 percent genes and 10 percent environment . There is no heritability in height for the individual.”

This distinction between group and individual is night and day. No marathon runner would calculate her own race time by averaging the race times of ten thousand other runners; knowing the average lifespan doesn’t tell me how long my life will be; no one can know how many kids you will have based on the national average. Averages are averages— they are very useful in some ways and utterly useless in others. It’s useful to know that genes matter, but it’s just as important to realize that twin studies tell us nothing about you and your individual potential. No group average will ever offer any guidance about individual capability.

In other words, there’s nothing wrong with the twin studies themselves. What’s wrong is associating them with the word “heritability,” which, as Patrick Bateson says, conveys “the extraordinary assumption that genetic and environmental influences are independent of one another and do not interact. That assumption is clearly wrong.” In the end, by parroting a strict “nature vs. nurture” sensibility, heritability estimates are statistical phantoms; they detect something in populations that simply does not exist in actual biology. It’s as if someone tried to determine what percentage of the brilliance of King Lear comes from adjectives. Just because there are fancy methods available for inferring distinct numbers doesn’t mean that those numbers have the meaning that some would wish for.

Kindle Locations 3551-3554

“The models suggest,” Turkheimer wrote, “that in impoverished families, 60% of the variance in IQ is accounted for by the shared environment, and the contributions of genes is close to zero; in affluent families, the result is almost exactly the reverse.” (Italics mine.) (Turkheimer et al., “Socioeconomic status modifies heritability of IQ in young children,” p. 632.)

Kindle Locations 2013-2074

These histones protect the DNA and keep it compact . They also serve as a mediator for gene expression, telling genes when to turn on and off. It’s been known for many years that this epigenome ( “epi-” is a Latin prefix for “above” or “outside”) can be altered by the environment and is therefore an important mechanism for gene-environment interaction.

What scientists didn’t realize, though, was that changes to the epigenome can be inherited. Prior to 1999, everyone thought that the epigenome was always wiped clean like a blackboard with each new generation.

Not so, discovered Enrico Coen. In the case of the Peloria toadflax flower, a clear alteration to the epigenome had subsequently been passed down through many generations.

And it wasn’t just flowers. That same year, Australian geneticists Daniel Morgan and Emma Whitelaw made a very similar discovery in mice. They observed that their batch of genetically identical mice were turning up with a range of different fur colors —differences traced back to epigenetic alterations and passed on to subsequent generations. What’s more, they and other researchers discovered that these fur-color epigenes could be manipulated by something as basic as food. A pregnant yellow mouse eating a diet rich in folic acid or soy milk would be prone to experience an epigenetic mutation producing brown-fur offspring, and even with the pups returning to a normal diet, that brown fur would be passed to future generations .

After that, more epigenetic discoveries piled in one after another:

  • In 2004, Washington State University’s Michael Skinner discovered that exposure to a pesticide in one generation of rats spurred an epigenetic change that led to low sperm counts lasting at least four generations.
  • In 2005, New York University’s Dolores Malaspina and colleagues discovered age-related epigenetic changes in human males that can lead to lower intelligence and a higher risk of schizophrenia in children.
  • In 2006, London geneticist Marcus Pembrey presented data from Swedish medical records to show that nutritional deficiencies and cigarette smoking in one generation of humans had effects across several generations .
  • In 2007, the Institute of Child Health’s Megan Hitchins and colleagues reported a link between inherited epigenetic changes and human colon cancer .

Welcome back, Monsieur Lamarck! “Epigenetics is proving we have some responsibility for the integrity of our genome,” says the Director of Epigenetics and Imprinting at Duke University, Randy Jirtle . “Before, [we thought that] genes predetermined outcomes. Now [we realize that] everything we do—everything we eat or smoke— can affect our gene expression and that of future generations. Epigenetics introduces the concept of free will into our idea of genetics.”

And that of future generations. This is big, big stuff— perhaps the most important discovery in the science of heredity since the gene.

No one can yet measure the precise implications of these discoveries, because so little is known. But it is already clear that epigenetics is going to radically alter our understanding of disease, human abilities, and evolution. It begins with this simple but utterly breathtaking concept:

Lifestyle can alter heredity.

Lamarck was probably not correct about the giraffe in particular, and he was certainly wrong about inherited characteristics being the primary vehicle of evolution. But in its most basic form, his idea that what an individual does in his/ her life before having children can change the biological inheritance of those children and their descendants— on this he turns out to have been correct. (And two hundred years ahead of everyone else.) Quietly, biologists have come to accept in recent years that biological heredity and evolution is a lot more intricate than we once thought. The concept of inherited epigenetic changes certainly does not invalidate the theory of natural selection, but it makes it a lot more complicated. It offers not just another mechanism by which species can adapt to changing environments, but also the prospect of an evolutionary process that is more interactive, less random, and runs along several different parallel tracks at the same time. “DNA is not the be all and end all of heredity,” write geneticists Eva Jablonka and Marion Lamb . “Information is transferred from one generation to the next by many interacting inheritance systems . Moreover, contrary to current dogma, the variation on which natural selection acts is not always random … new heritable variation can arise in response to the conditions of life.”

How do these recent findings impact our understanding of talent and intelligence? We can’t yet exactly be sure. But the door of possibility is wide-open. If a geneticist had suggested as recently as the 1990s that a twelve-year-old kid could improve the intellectual nimbleness of his or her future children by studying harder now, that scientist would have been laughed right out of the conference hall. Today, that preposterous scenario looks downright likely:

Washington, D.C.— New animal research in the February 4 [2009] issue of The Journal of Neuroscience shows that a stimulating environment improved the memory of young mice with a memory-impairing genetic defect and also improved the memory of their eventual offspring . The findings suggest that parental behaviors that occur long before pregnancy may influence an offspring’s well-being. “While it has been shown in humans and in animal models that enriched experience can enhance brain function and plasticity, this study is a step forward, suggesting that the enhanced learning behavior and plasticity can be transmitted to offspring long before the pregnancy of the mother,” said Li-Huei Tsai, PhD, at Massachusetts Institute of Technology and an investigator of the Howard Hughes Medical Institute, an expert unaffiliated with the current study.

In other words, we may well be able to improve the conditions for our grandchildren by putting our young children through intellectual calisthenics now.
What else is possible? Could a family’s dedication to athletics in one or more generations induce biological advantages in subsequent generations?
Could a teenager’s musical training improve the “musical ear” of his great-grandchildren?
Could our individual actions be affecting evolution in all sorts of unseen ways?

“People used to think that once your epigenetic code was laid down in early development, that was it for life,” says McGill University epigenetics pioneer Moshe Szyf. “But life is changing all the time, and the epigenetic code that controls your DNA is turning out to be the mechanism through which we change along with it. Epigenetics tells us that little things in life can have an effect of great magnitude.”

Everything we know about epigenetics so far fits perfectly with the dynamic systems model of human ability. Genes do not dictate what we are to become, but instead are actors in a dynamic process. Genetic expression is modulated by outside forces. “Inheritance” comes in many different forms: we inherit stable genes, but also alterable epigenes; we inherit languages, ideas, attitudes, but can also change them. We inherit an ecosystem, but can also change it.

Everything shapes us and everything can be shaped by us. The genius in all of us is our built-in ability to improve ourselves and our world.

Kindle Locations 1624-1657

To say that there is much we don’t control in our lives is a dramatic understatement, roughly on the order of saying that the universe is a somewhat large place. To begin with, there are many influences we can’t even detect. In 1999 , Oregon neuroscientist John C . Crabbe led a study on how mice reacted to alcohol and cocaine. Crabbe was already an expert on the subject and had run many similar studies, but this one had a special twist: he conducted the exact same study at the same time in three different locations (Portland , Oregon; Albany, New York; and Edmonton, Alberta) in order to gauge the reliability of the results. The researchers went to “extraordinary lengths” to standardize equipment, methods, and lab environment: identical genetic mouse strains, identical food, identical bedding, identical cages, identical light schedule, etc. They did virtually everything they could think of to make the environments of the mice the same in all three labs.

Somehow, though, invisible influences intervened. With the scientists controlling for nearly everything they could control, mice with the exact same genes behaved differently depending on where they lived. And even more surprising: the differences were not consistent, but zigged and zagged across different genetic strains and different locations. In Portland, one strain was especially sensitive to cocaine and one especially insensitive , compared to the same strains in other cities. In Albany, one particular strain— just the one— was especially lazy. In Edmonton , the genetically altered mice tended to be just as active as the wild mice, whereas they were more active than the wild mice in Portland and less active than the wild mice in Albany. It was a major hodgepodge.

There were also predictable results. Crabbe did see many expected similarities across each genetic strain and consistent differences between the strains. These were, after all, perfect genetic copies being raised in painstakingly identical environments. But it was the unpredicted differences that caught everyone’s attention. “Despite our efforts to equate laboratory environments, significant and, in some cases, large effects of site were found for nearly all variables,” Crabbe concluded. “Furthermore, the pattern of strain differences varied substantially among the sites for several tests.”

Wow. This was unforeseen, and it turned heads . Modern science is built on standardization; new experiments change one tiny variable from a previous study or a control group, and any changes in outcome point crisply to cause and effect. The notion of hidden, undetectable differences throws all of that into disarray. How many assumptions of environmental sameness have been built right into conclusions over the decades?

What if there really is no such thing? What if the environment turns out to be less like a snowball that one can examine all around and more like the tip of an iceberg with lurking unknowables? How does that alter the way we think about biological causes and effects?

Something else stood out in Crabbe’s three-city experiment : gene-environment interplay . It wasn’t just that hidden environmental differences had significantly affected the results. It was also clear that these hidden environments had affected different mouse strains in different ways— clear evidence of genes interacting dynamically with environmental forces.

But the biggest lesson of all was how much complexity emerged from such a simple model. These were genetically pure mice in standard lab cages. Only a handful of known variables existed between groups. Imagine the implications for vastly more complex animals— animals with highly developed reasoning capability, complex syntax, elaborate tools, living in vastly intricate and starkly distinct cultures and jumbled genetically into billions of unique identities. You’d have a degree of GxE volatility that would boggle any scientific mind— a world where, from the very first hours of life, young ones experienced so many hidden and unpredictable influences from genes, environment, and culture that there’d be simply no telling what they would turn out like.

Such is our world. Each human child is his/ her own unique genetic entity conceived in his/ her own distinctive environment , immediately spinning out his/ her own unique interactions and behaviors. Who among these children born today will become great pianists, novelists, botanists , or marathoners? Who will live a life of utter mediocrity? Who will struggle to get by? We do not know.

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16 thoughts on “Heritability & Inheritance, Genetics & Epigenetics, Etc

  1. As a notice, I blocked JayMan from my blog. He is one of the quasi-intellectual HBDers. He is friends with hbdchick, but he doesn’t have a fraction of her intellectual ability or her intellectual humility. That isn’t, however, the reason I blocked him.

    He wrote a comment that seemed to boil down to something closer to kneejerk denialism than to intellectual thoughtfulness. He doesn’t like the evidence that is coming out of this scientific field. It doesn’t fit his preconceived beliefs, assumptions and biases. He doesn’t like that science is more complex than his preferred ideology. So, he attacked my character and dismissed all that was inconvenient to his worldview.

    One of the greatest sins in my mind is denialism and even a whiff of it offends me. I admit that I don’t know a lot. I also admit that all of this is complex. JayMan also doesn’t know a lot, but he’d rather admit neither his lack of knowledge nor the complexity of the field. I will give him some credit that, when confronted with what he doesn’t know how to deny, he will on occasion grudgingly admit that the world doesn’t fit his preconceptions. The problem with this is that I don’t want to deal with people who have to be forced to admit the truth or even just admit uncertainty. Science is the wrong area of study for those demanding ideological certainty.

    I put truth before all else. I admit I don’t know or understand everything. I admit that in this post. Because of this, I’ve decided from now on I won’t interact with anyone who doesn’t share at least a basic level of intellectual humility. It just isn’t worth my time. I’ve already interacted with JayMan hundreds of times on this blog, on his blog and on hbdchick’s blog. Denialism is what I’ve come to expect of him. His recent comment that I blocked was simply the last straw.

    I’ve decided that to save my self time and grief I will no longer interact with denialists or other varieties of anti-intellectuals and pseudo-intellectuals. Disagreement of facts or interpretation is fine (including strong disagreement), but denialism is pointless. Denialists are like trolls. It is best not to feed them.

    This is a notice and a warning for anyone wishing to comment here or rather have their comment approved. If you wish to discuss, do so civilly and do so factually. Otherwise, this isn’t the place for you.

  2. I should point out that, despite his being far less impressive of a thinker compared to hbdchick, JayMan isn’t stupid. Many denialists aren’t stupid. Some are very smart and talented.

    JayMan is able to show his intellectual capacity, as long as it fits within his ideological beliefs. At those times, he can write some very interesting blogs. So, I’m not saying JayMan is intellectually worthless. It is because I was initially impressed with his wide interests that I later became disappointed by his moments of denialism; the denialism mainly coming up with issues of race.

    I disagree with JayMan on many things. Because of this, I’ve maybe disproportionately elicited his denialist side. This is just one small part of who he is, but from my perspective it is a very important aspect. Even if denialism only comes about certain issues, it still is just as problematic for those issues as if I were dealing with a religious fundamentalist.

    This is my reason for blocking him rather than just allowing his comment while ignoring it. I have an unofficial comment policy. If someone is worthy of commenting in my blog, they are worthy of a response by me. It basically came down to the realization that I could endlessly debate JayMan, but that would be fruitless and tiresome. Nothing could be achieved from it.

    I believe the world is more complex. JayMan believes the world is simpler. I’m wary of dogmatic ideology. JayMan has embraced dogmatic ideology. There is no way to bridge those differences in order to have an intellectual or even an interesting discussion.

    As an example of a different kind of interaction, I’m having a discussion with another person that I met from the HBD crowd, a group that does include some very interesting people. This other person is Staffan and the discussion we’re having is at this post:

    https://benjamindavidsteele.wordpress.com/2013/11/09/so-why-doesnt-the-united-states-fly-apart-at-the-seams/

    I disagree with him as well, but our discussion seems civil and intellectually honest. That is all I ask. In line with my unofficial policy, I feel compelled to give him worthy responses to his worthy comments.

    The reason have this unofficial policy is because it bothers me when I post at someone else’s blog and they offer no response, neither to disprove what I wrote nor to state where we may agree. It leaves a sense of inconclusiveness when you don’t know where someone stands. The point of blogging to me is to have worthy discussion, especially with those I disagree with. The key part, though, is that it is worthy.

  3. Let me note that, when I was writing this post, I was considering whether to mention HBDers like JayMan. I decided against it so as to keep it more neutral and more open to all involved. I didn’t want to make this about my disagreement with HBDers, but it obviously is directly related to human biodiversity.

    I specifically had bloggers like JayMan in mind while I was thinking about these issues. He demonstrates the problem I noticed with HBDers. The scientific understanding of most HBDers is certainly no better than my own understanding and usually far worse which is a truly sad state of affairs considering how minimal is my understanding.

    JayMan seems like a typical HBDer or race realist. He apparently doesn’t understand the difference between heritability and genetic inheritance and/or he doesn’t appreciate the implications of that distinction. I don’t think he is being disingenuous and obtuse. I’m fairly sure he is just a true believer, although of a mild variety.

    However, I want to be clear I wasn’t writing this post for the likes of JayMan. If he is fully committed to denialism, there is no way to reach him. Rather, I was providing this info for the type of person who might interact with someone like JayMan. I wanted to arm people with knowledge so that they won’t be suckerd in by pseudo-intellectual arguments. It is easy to cherrypick data as most HBDers do, but it is hard to genuinely try to grasp the complexity that doesn’t fit into ideological boxes.

  4. If you read a single thing in this post, the following bit will offer you an insight into the complexity many HBDers and race realists would ignore or try to rationalize away:

    Somehow, though, invisible influences intervened. With the scientists controlling for nearly everything they could control, mice with the exact same genes behaved differently depending on where they lived. And even more surprising: the differences were not consistent, but zigged and zagged across different genetic strains and different locations. In Portland, one strain was especially sensitive to cocaine and one especially insensitive , compared to the same strains in other cities. In Albany, one particular strain— just the one— was especially lazy. In Edmonton , the genetically altered mice tended to be just as active as the wild mice, whereas they were more active than the wild mice in Portland and less active than the wild mice in Albany. It was a major hodgepodge.

    Here is an experiment that is a million times more controlled than the best human studies. What makes this so devastating is that most HBDers and race realists aren’t even using the best human studies. They mostly rely on circumstantial evidence with very little to no controls of confounding factors.

    Genetics is more complex than human biodiversity theory can explain. When evidence and a theory contradict, I’d advise always go with the evidence.

    This isn’t to say that I’ve settled on a single other theory to explain this evidence for it is probably too early in the game for clear conclusions. My point is simpler. I’m not defending a particular view. I’m demanding HBDers and race realists be intellectually honest enough to deal with the contradictory data. I’ve known that, in their cherrypicking, most of them are unlikely to seek out this data. So, I posted it here. But even then someone like JayMan can’t face the writing on the wall. Science has passed him up and he tries the hold the ground of 20th century racialist/racist science.

    It is time we get serious about this kind of challenging evidence. We know a lot less than we thought we knew which wasn’t much in the first place. We are going to have to entirely revamp our understandings and our theories. This is no time for ideological gamemanship and political rhetoric.

    • Related to this study are several studies mentioned in another post of mine:

      https://benjamindavidsteele.wordpress.com/2013/11/11/black-superiority/

      “There are a total of seven studies providing direct evidence on the question of a genetic basis for the B/W IQ gap.”

      Those seven studies aren’t the type of studies focused on by HBDers and race realists. The reason they don’t focus on the direct evidence is becusese it contradicts their preferred conclusions/theories/beliefs.

      “Six of them are consistent with a zero genetic contribution to the gap (or with very slight African superiority) based just on the raw IQ numbers”

      Most of posts on HBD blogs are speculation, rather than discussion of the most well controlled scientific studies. If circumstantial and scientifically uncontrolled evidence is the best they can offer, it seems to show one how weak is their case.

  5. “In fact, The Bell Curve is extraordinarily one -dimensional. The book makes no attempt to survey the range of available data, and pays astonishingly little attention to the rich and informative history of this contentious subject. (One can only recall Santayana’s dictum, now a cliché of intellectual life: “Those who cannot remember the past are condemned to repeat it”). Virtually all the analysis rests upon a single technique applied to a single set of data— all probably done in one computer run.”

    Gould, Stephen Jay (2006-06-17). The Mismeasure of Man (Revised & Expanded) (Kindle Locations 6064-6068). W. W. Norton & Company. Kindle Edition.

  6. Here is another passage from one of the books in the above post:

    The Emperor’s New Clothes: Biological Theories of Race at the Millennium
    By Joseph L. Graves Jr.
    Kindle Locations 423-478

    The Impact of Natural Selection on the Genetic Composition of the Slaves

    There has been much speculation concerning how natural selection might have molded the characteristics of African Americans. Much of this speculation has occurred in the literature and popular myths concerning athletic performance. One much publicized racist comment was made by former CBS sports broadcaster Jimmy “The Greek” Snyder, who stated that the superior athletic ability of African Americans resulted from the fact that “blacks had been bred like race horses.” Although Snyder was fired soon after that broadcast, many people felt that Snyder was correct and that African American success in certain sports was directly linked to the biological results of slavery. In Taboo: Why Black Athletes Dominate Sports and Why We Are Afraid to Talk about It, Jon Entine concludes that genetic differences resulting from adaptation to local conditions might explain the dominance of “Blacks” in certain sports. However, he consistently confuses the concepts of local populations and socially constructed races, thus not completely escaping the race paradigm.

    The argument for African American superiority in sport proceeds as follows. The high mortality that must have resulted during the capture, warehousing, and transport of slaves must have selected stronger and healthier individuals. In addition, “seasoning” occurred once slaves arrived in the Americas, which might also have resulted in selection for disease resistance and physiological stamina. For example, there is strong evidence suggesting that innate immunity might have accounted for differential survival of Africans during the yellow fever epidemics that plagued much of the Caribbean. This example, however, is different from the general argument that suggests that slavery imposed a harsh regime that only the strongest and healthiest individuals survived. Enhanced physiological performance was consistently passed on to their offspring, hence accounting for the supposed superior athleticism observed in African Americans today.

    One other portion of the argument often goes unstated and unexamined: that is, the idea that the selection for disease resistance translates into superior athletic performance. If this were true, we could argue that the greater resistance of northern European populations to the AIDS virus is responsible for their dominance in speed skating, swimming, and downhill skiing.

    A corollary of the general argument is that the superior athletic performance of African Americans is negatively genetically correlated with intellectual performance. This is a variant of the hypothesis that reproductive performance is negatively correlated with intelligence, an idea spread by psychometrician J. Philippe Rushton. This corollary is severely flawed in several ways. The first flaw is the difficulty of reconstructing the actual conditions under which natural selection could have operated during slavery. Our ignorance about these conditions stems from our lack of strong historical interest in, or concern for, the actual nature of slavery and the rest of the African American experience. In addition, the argument suffers from the main fallacy of all adaptationist just-so stories: the assumption of genetic correlation between physiological performance and specific components of life history. We do not actually know, nor can we experimentally verify, how physiological performance was related to individual fitness during slavery (or even now). For example, a slave could have left more offspring by being intelligent, loyal, and honest or by being sly and morally corrupt. These behaviors might have little to no genetic cause and might be completely independent of physiological or athletic performance. Finally, this argument also lacks any foundation in the sociology of sport.

    Any conclusions about the action of natural selection during slavery must be speculative because the mortality data, both on sources and magnitudes, for all the various aspects of the trade are sketchy. For example, the mortality data from the slave ship Coningin Hester (Dutch registry, 1716, from West Africa to Caribbean), fail to show clear patterns.6 The ship carried a total of 183 female and 371 male slaves ranging in age from five to forty-four. Table 2.1 is a calculation of age-specific mortality rates for these individuals. One thing is clear. The data do not suggest that slave mortality on this voyage was mostly related to physiological performance. If human physiology were the sole factor in survival, we would expect to find the highest mortality rates among the oldest and the youngest age categories, which we know are most vulnerable to physiological stress. In addition, we would predict that female mortality would be greater than male mortality. However, we find instead that young adults experienced the highest mortality rates and that males died at about twice the rate of females.

    These data suggest instead that behavior, of both captives and slavers, rather than physiology might account for these patterns. Older captives may have survived through their greater experience and patience. Younger captives may have been given special care or quarters on the voyage (in part because of their future value and because they did not present a serious threat to the slavers). However, the mortality rates for both males and females were highest in the age categories that had the highest economic value. Because the years of prime reproduction coincide with the peak of physiological performance in animals, including humans, these slaves should have been the most capable of physiological resistance to the stress of the voyage and, thus, the most valuable to the slavers. Therefore, the high mortality in these age classes is a mystery. One possible explanation is that we see the highest mortality in the categories that were the most likely to resist their imprisonment. Male slaves were considered the most dangerous. Differential punishment, a condition that again depends on the behavior of both the captives and captors, could explain the twofold difference between male and female mortality rates. But we cannot insist on this explanation either. No simple explanation of survival patterns on this slave voyage can be made. In addition, the characteristics required to survive “seasoning” might have been very different from those required to survive any individual voyage. Consequently, any arguments concerning a specific mode of natural selection in shaping the genetic character of African Americans are likely to be fallacious.

    There is some need to clear up the confusion concerning the evolutionary processes responsible for gene frequencies in modern African Americans. Natural selection can be defined as the differential reproductive success of favored genotypes. (The genotype is specified by specific alleles found at particular loci.) Properly understood, success has both a survivorship and a reproductive component. However, natural selection alone is not sufficient to explain how changes in the genetic composition of a given population occur. We must also take into account the problem of accidents of genetic processes.

    We now know that sub-Saharan Africans have greater genetic variability than all other human populations combined.7 Slaves were drawn from all over Africa during the Atlantic trade. Those who came to the Americas were mainly from the West Coast. We have no reliable way today to determine the impact of the various sources of mortality during the slave trade on the victims’ gene frequencies. For example, we could argue that overweight individuals might have survived the Middle Passage better because of their greater fat stores or, conversely, that overweight people did not survive the process because of the cardiovascular stress caused by obesity.

    Certainly, we could argue that the entire process selected for individuals with great intelligence and mental flexibility. However, no one ever argues that African Americans have greater genetic potential for intelligence due to selection during slavery! No one argues that the rigors of being a slave owner, or the hardships of the westward migration in the United States, selected for greater athletic performance. The reason that these arguments are not advanced is that people hold the mistaken belief that only African Americans excel at certain sports. But sociologists of sport have shown that economic opportunity has a great deal to do with who ends up playing certain sports. In the late nineteenth century, many of the best boxers in the United States were of Irish and Italian extraction. Now these groups are rare in boxing. Even basketball was not always dominated by African American athletes. Jewish Americans were the first to succeed at the sport (it was thought that their “craftiness” made them better suited for the razzle-dazzle of the game).” If we wish to explain biological factors important to sports performance, we should look to body forms, not to race. For example, the Watusi people would be more likely to excel at basketball than the Pygmy, Yamamoto, or Aleut people because the former are very tall and the latter are short and stout. Body forms do not map racial categories in any consistent way.

  7. Also from Graves’ book, the following is the full context of the specific passage from the post above:

    The Emperor’s New Clothes: Biological Theories of Race at the Millennium
    By Joseph L. Graves Jr.
    Kindle Locations 2096-2210

    The Argument for the Link between Race and IQ

    Herrnstein and Murray base their claim for a genetic basis to the black-white differential in IQ on the following evidence: First, the National Longitudinal Survey of Youth 1979 found a 1.21 standard deviation difference favoring whites over blacks on the Armed Forces Qualifying Test (AFQT). The sample included 6,502 whites and 3,022 blacks (see figure 10.1). Herrnstein and Murray claim that this IQ difference is evidence of a genetic difference between whites and blacks at loci that influence IQ intelligence. They further support this claim by suggesting that this differential has been robust over the record of mental testing in the twentieth century.’ In addition, Herrnstein and Murray present data suggesting that the black-white differential does not disappear as one alters parental socioeconomic status.’ It is this sort of evidence that they marshal to substantiate the claim of an underlying genetic component for intelligence that differs between blacks and whites.

    For a moment, let us leave aside any questions about the quality of these data. Taking the data at face value, the naive observer might think that they support Herrnstein and Murray’s argument. However, to a professional geneticist their argument is utterly flawed. It is impossible from phenotypic data alone to apportion genetic and environmental sources of causality. Nor is the “robustness” of the data over the twentieth century any indication of genetic causality because the data do not take environmental effects into consideration. For example, pine trees growing on windy coasts show a characteristic twisted body form. As long as these populations live in this environment, the body form will persist. Take their seeds and plant them in a nonwindy environment and the “standard” non-twisted growth form is observed.

    Consider another example, this time from the insect world. Fruit flies maintained in the laboratory at 20° C live longer than genetically identical flies held at 25° C. The greater longevity persists over many generations with little genetic change resulting in the stocks.’ The data summarized in figure 10.1 are taken from only seventy-two years, or about two and one-half human generations. This is not enough time for any substantial change in a population of large size, unless it is subject to catastrophic mortality or infertility, which is demonstrably not the case here. It is very important to note that the mean IQ of both Euro-Americans and African Americans has increased by about 15 points (or 1 standard deviation) in the last thirty years (the Flynn effect).’° Recent data suggest that the rate of increase for average IQ scores became even greater in the 1980s (3.0 points per decade between 1932 and 1978, and 3.5 points between 1978 and 1989).” Herrnstein and Murray dismiss this fact by arguing that the increase is more likely a result of better testing than of a real change in mean IQ.”- Either way, this change indicates an environmental effect, since no significant genetic change could have occurred in this period. This magnitude of environmental effect demolishes the case for the use of raw IQ data as a source of genetic information.

    Such inconsistencies also demonstrate that the psychometricians have only an amateurish grasp of evolutionary genetics. Numerous errors flow from this lack of scientific perspective. The vast majority of Herrnstein and Murray’s evidence is based on phenotypic information; that is, the reputed difference between races is based on some indirect measure of cognitive function, usually a standardized test. The reliance on such tests is made worse by the fact that they have not been conclusively shown to properly measure intellectual function. From these tests, psychometricians infer an underlying genetic difference, despite the fact that standard quantitative genetic protocols are premised on the extensively corroborated demonstration that procedures such as theirs are scientifically invalid. The flaws in their research program are best illustrated in their obsession with the false association between “group heritability” and the necessity of racial differences in IQ. They presume they can show that IQ is inherited genetically and that there must be substantial genetically based differences between the races. Their focus on genetic predestination of intellectual ability is thus their rationale for supporting the status quo because, in their rather limited view, genes cannot be easily altered.

    Heritability in the Psychometric Worldview

    Much of the argument concerning racial differences in intelligence has focused on an inappropriate assumption, that is, the heritability of IQ. Throughout the debate on race and intelligence, the methodologies used to establish heritability have been fraught with error and fraud. Psychometricians often ignore basic difficulties in estimating quantitative genetic formulas for variation. The fact that IQ test scores have a continuous distribution indicates that whatever cognitive functions are related to these tests must be influenced by many genetic and environmental factors. The formal expression for heritability in the broad sense is simply the ratio of variance in the character due to genetic sources, over all sources of variance. Direct estimates of heritability in laboratory studies can be tedious. They require rigorous control of confounding environmental factors and careful measurements of the phenotype in question.

    Consider the equation for VP, the variance in the phenotype:

    VP = Vg + Ve + Vg X e + Cov(g,e) + Verroo

    where Vg = variance of genetic origin, Ve = variance of environmental origin, Vg X e = variance due to gene X environment interaction, Cov(g,e) = the covariance of genes and environment, and Verror = variance due to errors in measurement. This equation illustrates that one cannot infer that a phenotypic difference between two groups automatically indicates a genetic difference. Under laboratory conditions we can control the environment such that we can eliminate the third and fourth terms of the equation. For example, if we measure the longevity of fruit flies from two different populations and hold all environmental conditions the same for both groups, then we can safely assume that the third and fourth terms are close to zero. This leaves

    VP =Vg + Ve + Verror’

    If we have carefully measured the longevity phenotype, then we can assume that the difference between the two populations is indeed due to genetic sources. However, there is an additional caveat: before we can make these measurements we must rear the flies under identical conditions for at least two generations because complex phenotypes are strongly influenced by maternal environmental effects. The environmental conditions experienced during development can influence the expression of genes in the adult. It should be clear that none of the rigorous controls that are required to identify genetic effects in the laboratory exist under the conditions in which attempts to measure human IQ have been made.

    Psychometricians emphasize the heritability of intelligence. But the particular estimate of the heritability of intelligence, however defined, has little to do with the question of cognitive differences between races because the estimates used to calculate the heritability of intelligence result from studies of close relatives. We already know that most of the genetic variability in the human species is at the level of individuals or families. But family-level variation does not therefore translate directly into racial variation. Data from an experiment in my laboratory examining the effect of a known genetic substitution on the complex trait of longevity revealed significant variation in families within populations but no significant variation between the populations. That is, both populations had family genetic backgrounds that responded differentially to the genetic substitution when measured under rigorously controlled environmental conditions. This is another way of saying that if genes do influence intelligence, then we should expect that all races will have families that run the range of the genetic variability for intelligence. Thus, given the large genetic overlap of human populations, our expectation should be that there is no significant racial difference in intelligence or other behavioral traits.

    To this prediction the racists will howl, How then do you explain the persistent IQ differential reported by twentieth-century studies? The answer is elementary; let us look at the conditions under which the tests were given. Do they really adhere to the requirements of a valid test of genetic differentiation? Absolutely not.

    The problems of the psychometric program do not improve when it attempts to look at specific “genetic” systems reputedly associated with intelligence. After all, Arthur Jensen even admitted that there should be many genes that impact the expression of intelligence, precisely because it is a polygenic trait. It is significant that the psychometricians have been unable to properly define the physiological traits that are purportedly responsible for intelligence and that are differentiated among the racial groups. This lack of precision makes attempts at localizing the genes involved very difficult. For example, a recent study of genes associated with IQ in Chile found that the B allele of the A, B, 0 locus was correlated positively with IQ score in boys but negatively in girls.” The authors of the study were convinced that the large size of the statistical correlation guaranteed that they had uncovered a real genetic contribution made by this allele to intelligence. If these correlations were generally real, then we would expect to find a large variation within so-called racial groups for the genetic contribution to intelligence caused by the blood group alleles.

    Table 10.1, which shows the range of frequencies for the B allele in Africa, Asia, and Europe, indicates that there is a large overlap of the frequencies of the B allele among the populations of these regions. Therefore, if the impact of the B allele were independent of genetic background and environment, we would expect its genetic contribution to intelligence to be found in all races. Particularly interesting is the frequency of the B allele in purportedly genetically superior races. For example, in Europe, the English, Germans, and Swedes have very low frequencies of the B allele, 0.061, 0.08, and 0.07, respectively; whereas the “inferior” Slavs have high frequencies (Czechs and Yugoslavs at 0.222 and 0.143, respectively). In the United States, southern whites were shown to have a frequency of 0.05, and blacks a frequency of 0.129.” Thus this example of a genetic locus purportedly associated with higher intelligence contradicts the historical claims of the genetic inferiority of Slavs and Negroes relative to Nordics and American whites. For the psychometricians to maintain their support of genetic differences contributing to the intelligence variation among races, they would have to ignore results such as this. Alternatively, they could argue that complex genetic interactions, such as epistasis and gene X environment effects could account for the apparent discrepancies between the Chilean study and their historical quantifications of racial intelligence. However, if they admitted the latter point, they would also have to concede that these factors might make intractable the process of assigning causality for variation in intelligence to specific genetic loci for specific populations.

    In the end, the data that the psychometricians rely on to demonstrate racial difference in intelligence are simply the racial differences we already observe. William Shockley, for example, proposed that skin color was the metric by which we could measure intelligence-this despite no established physiological link between the loci that determine skin pigmentation and those that determine any aspect of mental functioning. Nor have the psychometricians been able to advance any credible evolutionary genetic mechanism to explain the origin of these consistent racial differences. We know that genetic differences among populations are created by the combined action of natural selection and genetic drift. The selection clines involved in producing human genetic variation differ independently from one another. There is no reason to suppose that these should have produced intellectual inferiority only in sub-Saharan Africans. Genetic drift cannot be invoked either, since drift events are random, and thus allelic variation related to intelligence that results from drift should also be scattered throughout human populations, as the case of the B allele illustrates. Thus, to explain the consistency of inferior IQs in sub-Saharan Africans, one would have to suppose some form of natural selection that was operating only on these populations. J. Philippe Rushton attempts to accomplish this by utilizing an r- and K-selection scenario to explain the life history features of the three major races. Briefly, he argues that the human races fall on the r- and K-continuum. The theory of r- and K-selection was devised in the late 1970s to address why some species had short lives and reproduced rapidly, while others had long lives and reproduced slowly. Examples of organisms on different ends of the scale would be weeds, which grow rapidly, but invest little in their bodily structures (r-selected) and trees, which grow slowly and invest large amounts in their structures (K-selected). According to Rushton’s view of the human races, Negroids are considered “weeds,” with high investments in reproduction, and thus less to invest in bodily structures such as brain mass, thereby having lower intelligence. Alternatively, Caucasoids and Asians are more “treelike,” with high investments in brain mass and thus greater intellect, and lower inputs to reproduction. I have examined his scenario and have argued that he fails.” This failure results from both an improper use of life history theory and a flawed analysis of the available data.

    The psychometric argument gets weaker when we examine the genetic variability within the human species, particularly the greater within-group than between-group variation. On solely genetic grounds one would expect these racial groups to be indistinguishable for a complex behavioral trait like intelligence. Indeed, even if intelligence were highly heritable, the establishment of differences in intellectual capacity among family groups within a supposed race would not mean that there would be differences among races. The argument for consistent genetic differentiation for IQ among races suffers from all of the points that I have raised. Each alone is a fatal error, and when taken together they invalidate the racist program of Shockley and his co-conspirators.

    The Ubiquity of Gene X Environment Interactions

    The most elementary requirement for a test of genetic differences between phenotypes is that they have been reared in and tested under the same environmental conditions. Meeting this requirement is not as easy as it seems, even with relatively simple traits. It is clear that no such equality of environmental conditions has existed or now exists for the races in the United States. In chapter 5, I discussed how the impact of hookworm infections on children varied depending on income and on soil type. We also know that the environmental conditions for African Americans were horrendous at the turn of the twentieth century. The entire history of the United States shows that the environment for African Americans has been consistently inferior to that for Euro-Americans. By necessity, that fact makes problematic any attempt to apportion genetic causality to any complex phenotype differing between these groups. For example, the scores on the AFQT surveyed by Herrnstein and Murray came from students who attended school systems that are still mostly segregated. Consider the segregation index for African Americans in the following cities (1993 data): Gary, Indiana, 89 percent; Detroit, 88 percent; Chicago, 86 percent; Cleveland, 86 percent; Milwaukee, 83 percent, Buffalo, 83 percent; St. Louis, 81 percent; Philadelphia, 80 percent; Cincinnati, 79 percent, and Birmingham, 79 percent. In the period from 1968 to 1992, between 67 and 76.6 percent of African American children attended schools with more than 50 percent minority enrollment. Numerous contemporary studies have shown that these segregated school districts are disadvantaged relative to white districts.’ Historical segregation and the unequal access to educational resources it caused are crucial in interpreting the results of standardized tests. Studies have shown that students’ scores on the mathematics portion of the SAT are strongly correlated with the number of mathematics courses they have taken in high school. Poor minority districts often have difficulty in attracting qualified mathematics and science teachers. Thus students in these areas probably, if not certainly, received lower quality instruction.

    There is also a growing awareness that minority populations are often forced to live in environments contaminated by toxic materials. We know that some of these materials affect the cognitive development of children who are exposed to them. For example, inner city children are often exposed to high levels of lead, which causes mental retardation and impaired growth; and children of farm laborers are exposed to high levels of pesticides with known neurotoxic impacts. As one might expect, racial composition is the best predictor of the location of hazardous waste facilities in the United States. This is true even when socioeconomic class is included in the statistical analysis. Thus, poor whites receive more toxic exposure than wealthy whites but less than poor racial minorities. This stratification means that many minority communities are literally on a toxic treadmill, with jobs in their communities being located in or near hazardous waste-producing industries or disposal sites. The problem of toxic materials and race in the United States is chilling in scope. Consider the following facts:

    • The nation’s largest landfill, which receives toxic materials from forty-five states and several foreign countries, is located in Sumter County, South Carolina, which is predominantly made up of poor African Americans.
    • The predominantly African American and Hispanic Southside of Chicago has the greatest concentration of hazardous wastes in the nation.
    • In Houston, Texas, six of the eight municipal dumps, and all five landfills, are located in predominantly African American neighborhoods.
    • In West Dallas, Texas, one African American neighborhood’s children suffered irreversible brain damage from exposure to lead at a nearby smelter. The residents won a $20 million out-of-court settlement.
    • Pesticide exposure among Hispanic farm workers causes more than three hundred thousand illnesses a year. A large percentage of these workers are children and women of childbearing age.

    There are more instances. Particularly illuminating is the percentage of African American population in the six cities that lead the list of cities with the highest number of hazardous waste sites (see table 10.2). Presently, 53 percent of the toxic waste sites located within one mile of public housing projects are located in communities that are greater than 75 percent minority (a total of 2,628 sites).’- These data are immediately relevant to the issue of innate racial differences in intelligence. A large sector of the African American and other minority populations are currently forced to live in poisonous environments. This is also reflected in the lower life expectancies of African Americans, as illustrated by their age-specific mortality (chapter 11). To be valid, any test of the genetic hypotheses of racial differences in intelligence must at least equalize the physical and educational environment of Euro-Americans and African Americans. The problem is not only that this experiment cannot be performed under the existing political circumstances but also that the proponents of the link between race and IQ do not argue that the experiment should be performed to test their hypotheses.

  8. You put all these writers with an ideological axe to grind, to prove the PC dogma.
    Like the geocentric planetary theory, the epicycles get more and more elaborate

    Rushton debunked various of these people.
    The theories get so elaborate and complex to distract from very simple facts. To deny the undeniable and obvious. Or to construct straw men and prove them false.

    Most of modern philosophy is build on such senseless complexity. Ever heard of Occam’s razor?

    • I realize that you’re ignorant. But it’s no excuse. You can find damning criticisms of Rushton’s unreliable data all over the internet and in scholarly books. I’ve even seen HBDers who share Rushton’s views be highly wary of his data. So, if that is the data you’re relying on, you need to better inform yourself. BTW Occam’s razor is based on the simplest explanation that takes into account all of the best data, not based on the most simpleminded ignorant belief.

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