The Language of Heritability

“The Minnesota twin study raised questions about the depth and pervasiveness of qualities specified by genes: Where in the genome, exactly, might one find the locus of recurrent nightmares or of fake sneezes? Yet it provoked an equally puzzling converse question: Why are identical twins different? Because, you might answer, fate impinges differently on their bodies. One twin falls down the crumbling stairs of her Calcutta house and breaks her ankle; the other scalds her thigh on a tipped cup of coffee in a European station. Each acquires the wounds, calluses, and memories of chance and fate. But how are these changes recorded, so that they persist over the years? We know that the genome can manufacture identity; the trickier question is how it gives rise to difference.”
~Siddhartha Mukherjee, Same But Different

If genetics are the words in a dictionary, then epigenetics is the creative force that forms those words into a library of books. Even using the same exact words in the genomic code from identical twins, they can be expressed in starkly different ways. Each gene’s expression is dependent on it’s relationship to numerous other genes, potentially thousands, and all of those genes together are moderated according to epigenetics.

The epigenome itself can be altered by individual and environmental factors (type of work, exercise, and injuries; traumatic abuse, chronic stress, and prejudice; smoking, drinking, and malnutrition; clean or polluted air, water and soil; availability of green spaces, socioeconomic class, and level of inequality; etc). Then those changes can be passed on across multiple generations (e.g., the grandchildren of famine victims having higher obesity rates). This applies even to complex behaviors being inherited (e.g., the grandchildren of shocked mice, when exposed to cherry blossom scent, still jumping in response to the shock their grandparents experienced when exposed to the same scent).

What is rarely understood is that heritability rates don’t refer directly to genetics alone. It simply speaks to the entire package of influences. We don’t only inherit genes for we also inherit epigenetic markers and environmental conditions, all of the confounders that make twin studies next to useless. Heritability is only meaningful at a population level and can say nothing directly about individual people or individual factors such as a specific gene. And at a population level, research has shown that behavioral and cultural traits can persist over centuries, and they seem to have been originally caused by distant historical events of which the living memory has long since disappeared, but the memory lingers in some combination of heritable factors.

Even if epigenetics could only last several generations, though at least in some species much longer, the social conditions could continually reinforce those epigenetic changes so that they effectively become permanently set. And the epigenetics, in predisposing social behaviors, would create a vicious cycle of feeding back into the conditions that maintain the epigenetics. Or think of the centuries-long history of racism in the United States where evidence shows racism remains pervasive, systemic, and institutional, in which case the heritability is partly being enforced upon an oppressed underclass by those with wealth, privilege, and power. That wealth, power, and privilege is likewise heritable, as is the entire social order. No one part can be disentangled from the rest for none of us are separate from the world that we are born into.

Now consider any given disease, behavior, personality trait, etc might be determined by thousands of genes, thousands of epigenetic markers, and thousands of external factors. Change any single part of that puzzle might mean to rearrange the the entire result, even leading to a complete opposite expression. The epigenome determines not only if a gene is expressed but how it is expressed because it determines how which words are used in the genomic dictionary and how those words are linked into sentences, paragraphs, and chapters. So, one gene might be correlated as heritable with something in a particular society while correlated to something entirely else in a different society. The same gene could potentially have immense possible outcomes, in how the same word could be found in hundreds of thousands of books. Many of the same words are found in both Harry Potter and Hamlet, but that doesn’t help us to understand what makes one book different from the other. This is a useful metaphor, although an aspect of it might be quite literal considering what has been proven in the research on linguistic relativity.

There is no part of our lives not touched by language in shaping thought and affect, perception and behavior. Rather than a Chomskyan language organ that we inherit, maybe language is partly passed on through the way epigenetics ties together genes and environment. Even our scientific way of thinking about such issues probably leaves epigenetic markers that might predispose our children and grandchildren to think scientifically as well. What I’m describing in this post is a linguistically-filtered narrative upheld by a specific Jaynesian voice of authorization in our society. Our way of speaking and understanding changes us, even at a biological level. We are unable of standing back from the very thing about which we speak. In fact, it has been the language of scientific reductionism that has made it so difficult coming to this new insight into human nature, that we are complex beings in a complex world. And that scientific reduction has been a central component to the entire ruling paradigm, which continues to resist this challenging view.

Epigenetics can last across generations, but it can also be changed in a single lifetime. For centuries, we enforced upon the world, often violently and through language, an ideology of genetic determinism and race realism. The irony is that the creation of this illusion of an inevitable and unalterable social order was only possible through the elite’s control of environmental conditions and hence epigenetic factors. Yet as soon as this enforcement ends, the illusion drifts away like a fog dissipated by a strong wind and now through clear vision the actual landscape is revealed, a patchwork of possible pathways. We constantly are re-created by our inheritance, biological and environmental, and in turn we re-create the social order we find. But with new ways of speaking will come new ways of perceiving and acting in the world, and from that a different kind of society could form.

[This post is based on what is emerging in this area of research. But some of it remains speculative. Epigenetics, specifically, is still a young field. It’s difficult to detect and follow such changes across multiple generations. If and when someone proves that linguistic relativity can even reach to the level of the epigenome, a seeming inevitability (considering it’s already proven language alters behavior and behavior alters epigenetics), that could be the death blow to the already ailing essentialist paradigm (Essentialism On the Decline). According to the status quo, epigenetics is almost too radical to be believed, as is linguistic relativity. Yet we know each is true to a larger extent than present thought allows for. Combine the two and we might have a revolution of the mind.]

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The Ending of the Nature vs Nurture Debate
Heritability & Inheritance, Genetics & Epigenetics, Etc
Identically Different: A Scientist Changes His Mind
Epigenetic Memory and the Mind
Inherited Learned Behavior
Epigenetics, the Good and the Bad
Trauma, Embodied and Extended
Facing Shared Trauma and Seeking Hope
Society: Precarious or Persistent?
Plowing the Furrows of the Mind

What If (Almost) Every Gene Affects (Almost) Everything?
by Ed Yong

But Evan Boyle, Yang Li, and Jonathan Pritchard from Stanford University think that this framework doesn’t go far enough.

They note that researchers often assume that those thousands of weakly-acting genetic variants will all cluster together in relevant genes. For example, you might expect that height-associated variants will affect genes that control the growth of bones. Similarly, schizophrenia-associated variants might affect genes that are involved in the nervous system. “There’s been this notion that for every gene that’s involved in a trait, there’d be a story connecting that gene to the trait,” says Pritchard. And he thinks that’s only partly true.

Yes, he says, there will be “core genes” that follow this pattern. They will affect traits in ways that make biological sense. But genes don’t work in isolation. They influence each other in large networks, so that “if a variant changes any one gene, it could change an entire gene network,” says Boyle. He believes that these networks are so thoroughly interconnected that every gene is just a few degrees of separation away from every other. Which means that changes in basically any gene will ripple inwards to affect the core genes for a particular trait.

The Stanford trio call this the “omnigenic model.” In the simplest terms, they’re saying that most genes matter for most things.

More specifically, it means that all the genes that are switched on in a particular type of cell—say, a neuron or a heart muscle cell—are probably involved in almost every complex trait that involves those cells. So, for example, nearly every gene that’s switched on in neurons would play some role in defining a person’s intelligence, or risk of dementia, or propensity to learn. Some of these roles may be starring parts. Others might be mere cameos. But few genes would be left out of the production altogether.

This might explain why the search for genetic variants behind complex traits has been so arduous. For example, a giant study called… er… GIANT looked at the genomes of 250,000 people and identified 700 variants that affect our height. As predicted, each has a tiny effect, raising a person’s stature by just a millimeter. And collectively, they explain just 16 percent of the variation in heights that you see in people of European ancestry.

An Enormous Study of the Genes Related to Staying in School
by Ed Yong

Over the past five years, Benjamin has been part of an international team of researchers identifying variations in the human genome that are associated with how many years of education people get. In 2013, after analyzing the DNA of 101,000 people, the team found just three of these genetic variants. In 2016, they identified 71 more after tripling the size of their study.

Now, after scanning the genomes of 1,100,000 people of European descent—one of the largest studies of this kind—they have a much bigger list of 1,271 education-associated genetic variants. The team—which includes Peter Visscher, David Cesarini, James Lee, Robbee Wedow, and Aysu Okbay—also identified hundreds of variants that are associated with math skills and performance on tests of mental abilities.

The team hasn’t discovered “genes for education.” Instead, many of these variants affect genes that are active in the brains of fetuses and newborns. These genes influence the creation of neurons and other brain cells, the chemicals these cells secrete, the way they react to new information, and the way they connect with each other. This biology affects our psychology, which in turn affects how we move through the education system.

This isn’t to say that staying in school is “in the genes.” Each genetic variant has a tiny effect on its own, and even together, they don’t control people’s fates. The team showed this by creating a “polygenic score”—a tool that accounts for variants across a person’s entire genome to predict how much formal education they’re likely to receive. It does a lousy job of predicting the outcome for any specific individual, but it can explain 11 percent of the population-wide variation in years of schooling.

That’s terrible when compared with, say, weather forecasts, which can correctly predict about 95 percent of the variation in day-to-day temperatures.

Complex grammar of the genomic language
from Science Daily

Each gene has a regulatory region that contains the instructions controlling when and where the gene is expressed. This gene regulatory code is read by proteins called transcription factors that bind to specific ‘DNA words’ and either increase or decrease the expression of the associated gene.

Under the supervision of Professor Jussi Taipale, researchers at Karolinska Institutet have previously identified most of the DNA words recognised by individual transcription factors. However, much like in a natural human language, the DNA words can be joined to form compound words that are read by multiple transcription factors. However, the mechanism by which such compound words are read has not previously been examined. Therefore, in their recent study in Nature, the Taipale team examines the binding preferences of pairs of transcription factors, and systematically maps the compound DNA words they bind to.

Their analysis reveals that the grammar of the genetic code is much more complex than that of even the most complex human languages. Instead of simply joining two words together by deleting a space, the individual words that are joined together in compound DNA words are altered, leading to a large number of completely new words.

“Our study identified many such words, increasing the understanding of how genes are regulated both in normal development and cancer,” says Arttu Jolma. “The results pave the way for cracking the genetic code that controls the expression of genes. “

What Genetics Does And Doesn’t Tell Us

I was looking at various articles and blogs on genetics, race, and IQ. I was also looking at the comments. It got me thinking about the quality of the public debate.

Much of the analysis and discussion is high quality. There are many people involved who are intelligent and well-read. But there still is a lot of misunderstanding and confusion about the issues of heritability, genetic inheritance, and shared environment. Without understanding these issues, there is no way to tackle all the related issues of race, IQ, etc.

This is a topic that I’ve posted about before. In that post, I offered many different perspectives from both online sources and books. If you check out some of the info from that post, you’ll realize how many complex factors are involved in a trait getting passed on and how difficult it is to determine causal relationships, specifically determining genetic influence.

This post is a continuation of what I shared there. I feel compelled to return to the topic because of its importance.

I’ll keep this post simpler, though. I’m only going to offer four articles for consideration, all of them from the website Science 2.0. There is no particular reason I’m offering these articles from this website other than that they caught my attention as I was browsing the web. The authors explain the issues well and I want to use this opportunity to promote their explanations.

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What Is Heritability?
By Gerhard Adam

“Heritability” is a term used in many articles and through much of the scientific literature and invariably promotes the idea that it relates specifically to inherited traits. As a result, it is often assumed that the heritability of a particular trait relates to how much influence genetics has on the trait manifesting in an individual.

However, that isn’t what it means.

Heritability attempts to address the relationship between nature (genetics) and nurture (environment), so that as each changes, the variation between individuals within a population can be estimated based on these influences. In this context, “environment” simply represents everything external to the genome that could effect expression.

Therefore the first significant aspect of heritability that must be understood is that it tells us nothing about individuals. It is strictly an estimate of the variations that occur within populations. If heritability is applied to an individual it is a meaningless concept [since an individual cannot be said to vary with anything].

It also doesn’t tell us anything about the specific influence of genes on any particular trait, since that would be the result of inheritance. We also need to understand that a trait is something that is “selectable”. In other words, there exists a possibility that outcomes can vary in the expression of a particular trait. This follows from the Mendelian view of inheritance where genes are represented as two alleles [dominant and recessive], so that particular combinations would produce certain outcomes. Therefore if there is no variation in the alleles, then everyone has the same genes and heritability would be zero. Adaptations like having a heart or a stomach are not selectable (too many genes and interactions) and therefore tell us nothing about heritability. The primary difference is that adaptations represent the cumulative effect of changes over time that have gone to fixation in a population. As a result, there is no “selection” that would determine “heart or no heart”. Therefore we can consider that the heart is an adaptation, while the risk of heart disease is a trait.

[ . . . . ]

One difficulty that arises with heritability is that any considered trait must be demonstrably linked to genetic transmission. This can become problematic when heritability is used to evaluate behavioral traits where the genetic link may be tenuous. In an effort to measure heritability, there is often a reliance on twin studies under the assumption that variances between them must be accountable to environment since they are effectively genetically identical. However, as previously mentioned, this can result in difficult interpretations when the traits in question are purely behavioral. Until such time as behavioral traits can be explicitly linked to genes, any statement regarding heritability must be considered suspect.

Heritability: A Primer
By Josh Witten

RED FLAG: If someone says the heritability of X is Y, then they probably don’t know what they are talking about.

Folks in the know, know that there are two kinds of heritability, broad sense and narrow sense. Those knowledgeable folks in the know are aware that it is extremely important to clearly state which heritability one is using, as the interpretation of each is different.

[ . . . . ]

Broad sense heritability tells us what proportion of the phenotypic variation is due to the genotypes of the individuals of the population. It tells us nothing about how similar the phenotype of a child will be to its parent. For that, we need the narrow sense heritability.

[ . . . . ]

Human behavioral studies, such as on IQ, have it much more difficult. Environmental variance is very difficult to control experimentally. Statistical methods can be used to correct for the effects of known environmental variables, but one cannot be certain that all variables have been accounted for. Without knowledge of the environmental variance, one cannot determine the value of Cov(G,E). Underestimating environmental variance and assuming, without evidence, that Cov(G,E)=0, will lead to an overestimation of Var(G), Var(A), and both broad and narrow sense heritability.

In this context, it becomes impossible to interpret either broad sense or narrow sense heritability rigorously. It is even questionable whether these metrics have any validity at all.

For a more thorough examination of the issue of heritability of IQ along these lines, I recommend dusting off a Science paper from 1974 by Layzer entitled “Heritability analyses of IQ scores: science or numerology?”.

What Our Genes Tell Us About Race
By Michael White

The debate over race and intelligence has a long and tarnished history, although that doesn’t mean it’s not a legitimate scientific question to address. However, the debate has taken place almost entirely outside modern genetics, falling instead within the realm of psychology (such as work done by Arthur Jensen). Some writers would have you believe that science is converging on a consensus that the ‘IQ’ gap between various races is genetic (and that liberal conspirators are trying to cover it up). That claim is false. Researchers have not identified a single genetic variant with an impact on intelligence that falls along population lines. In fact several studies have recently tested variants in genes that appear to be involved in controlling brain size. No correlation with intelligence was found. Yes, genetics does play a significant role in intelligence, and many other traits. But there is simply no genetic evidence (and I mean real genetics, not psychology) for genetic differences in intelligence between human populations.

Why is this so? Other traits, like skin color, obviously fall along population lines. While skin color is obviously not a 100% reliable predictor, skin color is a major indicator of race. Irish, Kenyans, Pakistanis, and Chinese populations all have clearly different skin tones.

It turns out, not surprisingly, that the genetic variation for some (but not all) skin color genes does in fact follow population divisions, in contrast with most other genetic variation. This is most likely because skin color differences end up being relatively simple – a single variant of a gene (causing lighter skin, for example) can easily become common in a population through natural selection. The result is that you have different human populations with dramatic differences in skin color.

Other traits, however, are much more complex than skin color. Physical differences which are determined not by one, but many different genetic variants, are unlikely to split neatly by population. Intelligence is probably one of the most complex traits humans possess. It is almost certainly affected by variants in many different genes, and many of those genes have other important functions in the body. That means this: two different human populations could have easily developed differences in skin color between them, but differences in intelligence would have been extremely hard to develop, by chance or by natural selection.

Racial conflict has long been a part of human societies. Along with that conflict has come frequent speculation (most famously, but not exclusively among whites with European ancestry) that one race is inferior to another. Some have been worried that modern genetics would substantiate that belief, but our best genetic evidence to date shows those worries unfounded. Genetics does play a large role in the diversity we find among human beings. That diversity, in spite of some dramatic but superficial exceptions like skin color, is shared in common among all races.

Why Race Is Pseudo-Science
By Gerhard Adam

However, the premise is quite simple. If you can’t actually define it in scientific terms, then it cannot be science. Therefore any claims that derive from it are not science. Similarly, we cannot claim that “race” is valid by simply engaging in arm-waving arguments based on the fact that there are genetic differences between various population groups. “Race” must be fully quantifiable as specific heritable trait(s) that serves to identify the group in question.

[ . . . . ]

If the concept of race is to be scientific, then it would need to specifically identify the genetic criteria that is to be used for that differentiation. Merely claiming some external trait isn’t going to do it.

Such simplistic thinking is insufficient to raise the idea of “race” beyond anything except another convenient [or inconvenient as the case may be] cultural grouping.

[ . . . . ]

So, if we really want to pursue the topic of “race” or designating subspecies of humans, then lets do so on a scientific basis, and not some arbitrary socio-cultural designation. If “race” is going to be based on genetics, then it should be intuitively obvious that people will have their “racial” classification changed based solely on their personal family history. As a result, the designation of any particular “race” could actually change from generation to generation. Therefore any claim at racial knowledge that is based on arbitrary external traits rather than the specific genetic traits, is, by definition, wrong 7.

Show me the genes.

Click to access 11076233.pdf

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.

* * * * *

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

* * * * *

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).

* * * * *

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.

* * * * *

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

* * * * *

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.

* * * * *

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.

* * * * *

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.

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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.

Will you cheat? Check your fingers

Finger length may reveal your financial acumen
By Linda Geddes

He found that traders with a longer ring fingers, and therefore higher prenatal testosterone, made on average six times the profits of traders exposed to low levels of the hormone, and tended to remain traders for longer.

Previous studies have also suggested a link between a low index-to-ring-finger ratio and autism, and better sporting ability.

“This study provides evidence for human beings of what we know from studies of animals, that exposure to sex hormones early in life predisposes the nervous systems and resulting behavior to develop in certain ways,” says Bruce mcEwen of the Rockefeller University in New York. “In this case the development of the risk taking, visual-motor skills, etc that make for success in this kind of rapid stock trading.”

Finger Length Key to Female Athletic Potential

“Previous studies have suggested the change in finger length was due to changes in testosterone levels in the womb,” he said.
But he said the unit had found in a separate study of twins that finger length was largely inherited, possibly explaining why sporting parents often have sporting children.
“We found that finger length was 70 percent heritable with little influence of the womb environment,” he said.
“This suggests that genes are the main factor and that finger length is a marker of your genes.”