PRIMARY SOURCES
My understanding of how genes work and traits develop comes from hundreds of books and articles. The most important (in alphabetical order) are as follows:
Bateson, Patrick, and Paul Martin. Design for a Life: How Biology and Psychology Shape Human Behavior. Simon & Schuster, 2001.
Bateson, Patrick, and Matteo Mameli. “The innate and the acquired: useful clusters or a residual distinction from folk biology?” Developmental Psychobiology 49 (2007): 818–31.
Godfrey-Smith, Peter. “Genes and Codes: Lessons from the Philosophy of Mind?” In Biology Meets Psychology: Constraints, Conjectures, Connections, edited by V. Q. Hardcastle. MIT Press, 1999, 305–31.
Gottlieb, Gilbert. “On making behavioral genetics truly developmental.” Human Development 46 (2003): 337–55.
Griffiths, Paul. “The Fearless Vampire Conservator: Phillip Kitcher and Genetic Determinism.” In Genes in Development: Rereading the Molecular Paradigm, edited by E. M. Neumann-Held and C. Rehmann-Sutter. Duke University Press, 2006.
Jablonka, Eva, and Marion J. Lamb. Evolution in Four Dimensions. MIT Press, 2005.
Johnston, Timothy D., and Laura Edwards. “Genes, interactions, and the development of behavior.” Psychological Review 109, no. 1 (2002): 26–34.
McClearn, Gerald E. “Nature and nurture: interaction and coaction.” American Journal of Medical Genetics 124B, no. 1 (2004): 124–30.
Meaney, Michael J. “Nature, nurture, and the disunity of knowledge.” Annals of the New York Academy of Sciences 935 (2001): 50–61.
Moore, David S. The Dependent Gene: The Fallacy of “Nature vs. Nurture.” Henry Holt, 2003.
Oyama, Susan, Paul E. Griffiths, and Russell D. Gray. Cycles of Contingency: Developmental Systems and Evolution. MIT Press, 2003.
Pigliucci, Massimo. Phenotypic Plasticity: Beyond Nature and Nurture. Johns Hopkins University Press, 2001.
Ridley, Matt. Nature via Nurture. HarperCollins, 2003.
Rutter, Michael, Terrie E. Moffitt, and Avshalom Caspi. “Gene-environment interplay and psychopathology: multiple varieties but real effects.” Journal of Child Psychology and Psychiatry 47, no. 3/4 (2006): 226–61.
Turkheimer, Eric. “Three laws of behavior genetics and what they mean.” Current Directions in Psychological Science 9, no. 5 (October 2000): 160–64.
While it would be impossible to further rank the above works in terms of their brilliance or general importance, I must give special credit to Matt Ridley’s Nature via Nurture for its importance in laying down a basic new foundation of knowledge of gene-environment interaction. Which does not, of course, mean that Ridley should get blamed for any of my silly mistakes …
CHAPTER NOTES
And to think [I’m] the cause of it: Chase and Winter, “The Sopranos: Walk Like a Man,” May 6, 2007.
The irony is that as America equalizes the [environmental] circumstances: Herrnstein and Murray, The Bell Curve, p. 91.
There’s also this gem: “Universal college education cannot be. Most people are not smart enough to profit from an authentic college education.” (Murray and Seligman, “As the Bell Curves.”)
“There are no genetic factors that can be studied independently of the environment.”
He uses “phenotype” instead of “a trait.” I substituted so as not to distract the reader. Here’s the original quote: “There are no genetic factors that can be studied independently of the environment, and there are no environmental factors that function independently of the genome. Phenotype emerges only from the interaction of gene and environment.” Meaney continues: “The search for main [direct] effects is a fool’s errand. In the context of modern molecular biology, it is a quest that is without credibility.” (Meaney, “Nature, Nurture, and the Disunity of Knowledge,” pp. 50–61.)
We’ve all been taught that we inherit complex traits like intelligence straight from our parents’ DNA in the same way we inherit simple traits like eye color. This belief is continually reinforced by the popular media.
A few examples:
“An organism’s physiology and behaviour are dictated largely by its genes,” the Economist declared in 1999. (Griffiths, “The Fearless Vampire,” p. 4.)
In 2005, Scientific American affirmed: “Even such abstract qualities as personality and intelligence are coded for in our genetic blueprint.” (Gazzaniga, “Smarter on Drugs,” p. 32.)
On November 11, 2008, as the writing of this book was drawing to a close, the New York Times published a remarkable piece by Carl Zimmer acknowledging a revolutionary new understanding of genes. Some key excerpts:
The familiar double helix of DNA no longer has a monopoly on heredity. Other molecules clinging to DNA can produce striking differences between two organisms with the same genes. And those molecules can be inherited along with DNA … It turns out, for example, that several different proteins may be produced from a single stretch of DNA … It turns out that the genome is also organized in another way, one that brings into question how important genes are in heredity. Our DNA is studded with millions of proteins and other molecules, which determine which genes can produce transcripts and which cannot. New cells inherit those molecules along with DNA. In other words, heredity can flow through a second channel. (Zimmer, “Now: The Rest of the Genome.”)
Still, the online New York Times health guide, under the heading “Genetics,” crudely states: “It is common knowledge that a person’s appearance—height, hair color, skin color, and eye color—are determined by genes. Mental abilities and natural talents are also affected by heredity, as is the susceptibility to acquire certain diseases.”
Think of your own genetic makeup: Friend, “Blueprint for Life,” p. D 01
Gregor Mendel demonstrated that basic traits: Field Museum, “Gregor Mendel: Planting the Seeds of Genetics.”
Mendel had proved the existence of genes—and seemed to prove that genes alone determined the essence of who we are. Such was the unequivocal interpretation of early-twentieth-century geneticists.
Pitzer College’s David S. Moore provides a nice capsule history of genetic determinism from the time of Mendel:
The idea that genetic factors might be able to determine the form of biological and psychological traits has been with us since the beginning of modern theorizing about genes. Although Gregor Mendel did not use the word genes to name the ‘heritable factors’ that he inferred must be responsible for observed variations in his experimental pea plants, the notion of a deterministic ‘germ plasm’ had appeared in several late 19th century writings on biology—most notably in the work of August Weismann—and because of the close conceptual similarity between Mendel’s ‘heritable factors’ and Weismann’s deterministic ‘germ plasm,’ it is little wonder that just a few decades later, Mendel’s factors came to be thought of as deterministic ‘genes.’ T. H. Morgan’s early 20th century discovery that genes are located on chromosomes eventually led to the development of the modern gene theory, which holds that genes are responsible for the development of inherited traits; this conclusion was based on the finding that the presence of particular genetic factors is highly correlated with the presence of particular traits. But even though such correlations do not support the contention that genes operate deterministically, modern gene theory nonetheless retained the genetic determinism that 19th century ‘germ plasm’ theorists relied on to explain the intergenerational transmission of evolutionarily adaptive characteristics. This sort of conceptualization continued to inform theoretical biology well past the middle of the 20th century, as biologists embraced Francois Jacob and Jacques Monod’s operon model of how genes regulate development. (Moore, “Espousing interactions and fielding reactions,” p. 332.)
Moore also notes that Johannsen recognized that development was a factor, and that they were ignoring development with their genes-only approach. (Moore, The Dependent Gene, p. 167.)
“It’s in the genes,” we say.
What makes Michael Phelps such an outstanding swimmer? It’s “all about gene pool,” quips syndicated sports columnist Rob Longley. “Phelps [has been] blessed with so many gifts, he is nothing short of a freak of nature.” (Longley column.)
over the last two decades Mendel’s ideas have been thoroughly upgraded—so much so that one large group of scientists now suggests that we need to wipe the slate clean and construct an entirely new understanding of genes.
Ironically, as this sweeping new view of how genes work has emerged, it has received little public attention. Front-page headlines still trumpet advances in gene splicing, genome mapping, gene testing, cloning, and so on. The result has been a growing public disconnect between genetic understanding and genetic reality. The public has gotten the impression that the answer to almost every question about our health and well-being can be found in our genome. The reality is a lot more nuanced.
Not all of the interactionists’ views have yet been fully accepted.
This book is not a dispassionate presentation of all scientific points of view. Instead, it embraces the arguments of the Interactionists, whose views I came to trust most after much reading, conversation, and consideration.
One brief description of the running disagreement can be found in Johnson and Karmiloff-Smith, “Neuroscience Perspectives on Infant Development,” which may be accessed online via Google Books (go to “Contents,” and click).
Another comes from Patrick Bateson and Matteo Mameli:
Many authors writing today suppose that innateness has something to do with genes (e.g., Tooby & Cosmides, 1992; Plotkin, 1997; Chomsky, 2000; Fodor, 2001; Pinker, 1998, 2002; Miller, 2000; Baron-Cohen, 2003; Buss, 2003; Marcus, 2003; Marler, 2004). In some cases, this supposition is based on imprecise ways of thinking about the role of genes in development. To argue, for instance, that a phenotype is innate if and only if genes and nothing but genes are required for its development is too simplistic. No phenotype is such that only genes are needed for its development, since an interplay between the organism and its environment is required at all stages of development. (Bateson and Mameli, “The innate and the acquired,” p. 819.)
“The popular conception of the gene as a simple causal agent is not valid,” declare geneticists Eva Jablonka and Marion Lamb.
They add: “[Geneticists now] recognize that whether or not a trait develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule[s], and the environment in which an individual develops.”
Also: “The idea that there is a gene for adventurousness, heart disease, obesity, religiosity, homosexuality, shyness, stupidity, or any other aspect of mind or body has no place on the platform of genetic discourse.” (Jablonka and Lamb, Evolution in Four Dimensions, pp. 6–7.)
This obliterates the long-standing metaphor of genes as blueprints with elaborate predesigned instructions for eye color, thumb size, mathematical quickness, musical sensitivity, etc.
Deploying the right metaphor is everything in the communication and understanding of science. In the case of genetics, our metaphors have sadly led us astray. “There is no clear, technical notion of ‘information’ in molecular biology,” writes biologist and philosopher Sahotra Sarkar. “It is little more than a metaphor that masquerades as a theoretical concept and … leads to a misleading picture of possible explanations in molecular biology.”
Today’s popular understanding of genes, heredity, and evolution is not just crude; it is profoundly misleading. It may feel true, thanks to the elegance of the “blueprint” and “code” metaphors, and thanks to the lack of a cogent dissent. But from the vantage of twenty-first-century scientific understanding, any brand of genetic determinism obscures more than it enlightens. We’ve created a thick, semipermanent veil that shrouds the more interesting, and more hopeful, reality.
“What we need here,” writes John Jay College’s Susan Oyama (a leader in the dynamic systems movement), “is the stake-in-the-heart move, and the heart is the notion that some influences are more equal than others, that form, or its modern agent, information, exists before the interactions in which it appears and must be transmitted to the organism either through the genes or by the environment.” (Oyama, The Ontogeny of Information, p. 27.)
genes—all twenty-two thousand of them—are more like volume knobs and switches.
This is my attempt to come up with a metaphor that will resonate and that accurately captures the dynamic quality of genes.
Estimates of the actual number of genes vary.
Although the completion of the Human Genome Project was celebrated in April 2003 and sequencing of the human chromosomes is essentially “finished,” the exact number of genes encoded by the genome is still unknown. October 2004 findings from the International Human Genome Sequencing Consortium, led in the United States by the National Human Genome Research Institute (NHGRI) and the Department of Energy (DOE), reduce the estimated number of human protein-coding genes from 35,000 to only 20,000–25,000, a surprisingly low number for our species. Consortium researchers have confirmed the existence of 19,599 protein-coding genes in the human genome and identified another 2,188 DNA segments that are predicted to be protein-coding genes. In 2003, estimates from gene-prediction programs suggested there might be 24,500 or fewer protein-coding genes. The Ensembl genome-annotation system estimates them at 23,299. (Human Genome Project, “How Many Genes Are in the Human Genome?”)
Also: New data “threaten to throw the very concept of ‘the gene’—either as a unit of structure or as a unit of function—into blatant disarray.” (Keller, The Century of the Gene, p. 67.)
Many of those knobs and switches can be turned up/down/on/off at any time—by another gene or by any minuscule environmental input. This flipping and turning takes place constantly.
Experiential factors are now known to influence gene expression through several mechanisms, including (but not limited to) those involving the actions of steroid hormones … For example, testosterone levels change as a function of sexual experience, and hormones like testosterone are known to be able to diffuse across both cellular and nuclear membranes where—once they have been bound by specific receptors—they can bind with DNA to regulate gene expression. (Moore, “Espousing interactions and fielding reactions,” p. 340.)
this process of gene-environment interaction drives a unique developmental path for every unique individual.
“The process of GxE acting over a lifetime may be the key to understanding much of human complex trait variability.” (Brutsaert and Parra, “What makes a champion?” p. 110.)
This may sound crazy at first, because of how thoroughly we’ve been indoctrinated with Mendelian genetics. The reality turns out to be much more complicated—even for pea plants.
Mendel’s pea-plant example has a built-in logical flaw: by assuring a consistent environment, it eliminates any visible environmental impact on heredity. When the environment is perfectly consistent from plant to plant, it does indeed appear that genes single-handedly determine heredity. This is akin to throwing dice, but instead of rolling two dice at once, keeping one of them permanently on 6. The second die is always going to determine the total.
Many scientists have understood this much more complicated truth for years but have had trouble explaining it to the general public. It is indeed a lot harder to explain than simple genetic determinism.
In a 2009 essay for the New York Times Magazine, Steven Pinker writes: “For most … traits, any influence of the genes will be probabilistic. Having a version of a gene may change the odds, making you more or less likely to have a trait, all things being equal, but as we shall see, the actual outcome depends on a tangle of other circumstances as well.” (Italics mine.)
While this is important acknowledgment that most genes do not determine traits directly, the use of the word “probabilistic” is crude and troublesome in two ways: First, it gives a new wrong impression about how genes work—making them sound like dice. Second, it misses a critical opportunity to help the general public understand genetic expression and gene-environment interaction.
The term “probabilistic” is meant to convey the understanding that most specific gene variants (alleles) do not guarantee certain outcomes. That much is true.
But the term goes much further. It also conveys the strong sense that a certain gene creates a specific probability that a person will develop a certain trait. That is very misleading—as Pinker himself demonstrates.
To explore the current state of genetics, Pinker had his own DNA analyzed. Among other things, it was revealed that he had the T version of a gene called rs2180439 SNP. As it turns out, 80 percent of men with the T version of this gene are bald. Pinker has a head full of curly gray hair. “Something strange happens when you take a number representing the proportion of people in a sample and apply it to a single individual,” he writes. “The first use of the number is perfectly respectable as an input into a policy that will optimize the costs and benefits of treating a large similar group in a particular way. But the second use of the number is just plain weird.”
Exactly. And that is also, in my opinion, why it is a bad idea to use the word “probabilistic” to describe the nature of genes. Genes don’t always lead to certain outcomes, because they are involved in a complex gene-environment dynamic. For the exact same reason, genes also don’t create a specific probability of an outcome.
My argument with the term “probabilistic” is not an argument against population genetics research. Such studies can be darn useful in setting medical policy, as Pinker suggests. But such studies should not drive our descriptive terminology for genes and how they work. (Quotes from Pinker, “My Genome, My Self.”)
Proteins are large, specialized molecules that help create cells, transport vital elements, and produce necessary chemical reactions.
From the online Genetics Home Reference guide:
What are proteins and what do they do?
Proteins are large, complex molecules that play many critical roles in the body. They do most of the work in cells and are required for the structure, function, and regulation of the body’s tissues and organs. Proteins are made up of hundreds or thousands of smaller units called amino acids, which are attached to one another in long chains. There are 20 different types of amino acids that can be combined to make a protein. The sequence of amino acids determines each protein’s unique 3-dimensional structure and its specific function. Proteins can be described according to their large range of functions in the body, listed in alphabetical order:
Examples of protein functions
Antibody: Antibodies bind to specific foreign particles, such as viruses and bacteria, to help protect the body.
Enzyme: Enzymes carry out almost all of the thousands of chemical reactions that take place in cells. They also assist with the formation of new molecules by reading the genetic information stored in DNA.
Messenger: Messenger proteins, such as some types of hormones, transmit signals to coordinate biological processes between different cells, tissues, and organs.
Structural component: These proteins provide structure and support for cells. On a larger scale, they also allow the body to move.
Transport/storage: These proteins bind and carry atoms and small molecules within cells and throughout the body.
This explains how every brain cell and hair cell and heart cell in your body can contain all of your DNA but still perform very specialized functions.
Lawrence Harper writes:
Every cell inherits a full nuclear complement of DNA. That is, all cells in the organism have the same potential. In the presence of appropriate external conditions, what underlies the development of multicellular organisms is a progressive, differential production (expression) of certain subsets of this genetic potential in different tissues … The features of each tissue type are thus determined by the pattern of gene expression, the genes in the cells that are “turned on” or “off” or show distinctive rates of production of gene products. (Harper, “Epigenetic inheritance and the intergenerational transfer of experience,” p. 344.)
“Development is chemistry”: Brockman, “Design for a Life: A Talk with Patrick Bateson.”
All of this means that, on their own, most genes cannot be counted on to directly produce specific traits. They are active participants in the developmental process and are built for flexibility. Anyone seeking to describe them as passive instruction manuals is actually minimizing the beauty and power of the genetic design.
Lawrence Harper writes:
Of particular relevance to the understanding of behavioral ontogeny is the fact that, in the process of development, cellular gene expression can be stably altered in response to conditions outside the organism to permit it to adapt to its environment. That is, not only do cells differentiate (specialize in function) in response to external signals, but once so differentiated, their subsequent functional activity as, for example, nerves or glandular tissue, also can be modified at the molecular level. Probably the most obvious example of such altered activity of specialized cells is the development of immunity to pathogens. (Harper, “Epigenetic inheritance and the intergenerational transfer of experience,” p. 345.)
“Even in the case of eye color,” says Patrick Bateson, “the notion that the relevant gene is the [only] cause is misconceived, because [of] all the other genetic and environmental ingredients.” (Italics mine). Bateson, “Behavioral Development and Darwinian Evolution,” p. 149.
A taste of the complexities behind eye color, from three different sources:
Iris color was one of the first human traits used in investigating Mendelian inheritance in humans. Davenport and Davenport (1907) outlined what was long taught in schools as a beginner’s guide to genetics, that brown eye color is always dominant to blue, with 2 blue-eyed parents always producing a blue-eyed child, never one with brown eyes. As with many physical traits, the simplistic model does not convey the fact that eye color is inherited as a polygenic, not as a monogenic, trait (Sturm and Frudakis, 2004). Although not common, 2 blue-eyed parents can produce children with brown eyes. (McKusick, “Eye Color 1.”)
Human iris color is a quantitative, multifactorial phenotype that exhibits quasi-Mendelian inheritance … To identify genetic features for best-predicting iris color, we selected sets of SNPs by parsing P values among possible combinations … These results confirm that OCA2 is the major human iris color gene and suggest that using an empirical database-driven system, genotypes from a modest number of SNPs within this gene can be used to accurately predict iris melanin content from DNA. (Frudakis, Terravainen, and Thomas, “Multilocus OCA2 genotypes specify human iris colors,” pp. 3311–26.)
The highest association for blue/nonblue eye color was found with three OCA2 SNPs … The TGT/TGT diplotype found in 62.2% of samples was the major genotype seen to modify eye color, with a frequency of 0.905 in blue or green compared with only 0.095 in brown eye color. This genotype was also at highest frequency in subjects with light brown hair and was more frequent in fair and medium skin types, consistent with the TGT haplotype acting as a recessive modifier of lighter pigmentary phenotypes. (Duffy et al., “A three-single-nucleotide polymorphism haplotype in intron 1 of OCA2 explains most human eye-color variation,” p. 241.)
Single-gene diseases do exist and account for roughly 5 percent of the total disease burden in developed countries: Khoury, Yang, Gwinn, Little, and Flanders, “An epidemiological assessment of genomic profiling for measuring susceptibility to common diseases and targeting interventions,” Hall, Morley, and Lucke, “The prediction of disease risk in genomic medicine.”
Susan Brooks Thistlethwaite adds:
Genetics is not merely a matter of single gene disorders or single gene traits, such as flower color and pod shape in Mendel’s pea plants. Mendelian genetics is about single gene disorders [that] occur in only 3 percent of all individuals born alive …
Human inheritance is much more complicated. Most conditions are polygenic (involve many genes), and their expression depends on gene-gene and environment-gene interactions. (Thistlethwaite, Adam, Eve, and the Genome, p. 70.)
“A disconnected wire can cause a car to break down”: Oyama, Griffiths, and Gray, Cycles of Contingency, p. 157.
“Genes store information coding for the amino acid sequences of proteins,” explains Bateson. “That is all”: Bateson, Design for a Life, p. 66.
Similar statement: “All the genes can code for, if they code for anything, is the primary structure (amino acid sequence) of a protein.” (Godfrey-Smith, “Genes and Codes,”. p. 328)
One of the most striking early hints of the new understanding of development as a dynamic process emerged in 1957.
There were much earlier hints. “For most of the past century,” says Penn State geneticist Gerald E. McClearn, “the evidence has been clear that a more collaborative model of coaction and interaction of genetic and environmental agencies is more appropriate. Even in the pell-mell pursuit of Mendelian phenomena in the post-rediscovery enthusiasm at the beginning of the last century, examples of the interdependence of genetic and environmental influences surfaced. One well-known early example is that of Krafka [1920], who showed that the effect of the bar-eyed genotype (now known to be a duplication) on eye facet number of Drosophila is strikingly dependent on the temperature at which the flies are maintained.” (McClearn, “Nature and nurture,” p. 124.)
heights of Japanese children: Greulich, “A comparison of the physical growth and development of American-born and native Japanese children,” p. 304.
Greulich didn’t realize this at the time, but it was a perfect illustration of how genes really work: not dictating any predetermined forms or figures, but interacting vigorously with the outside world to produce an improvised, unique result.
Two excellent summaries from two of the top figures in the field of gene-environment interaction:
A key feature of gene expression is that it can be altered in a reversible way by extra-cellular signals and by environmental influences. Although DNA starts off the causal chain, what really matters is the expression of the genes (in terms of messenger RNA). There are no genetic effects without this expression. (Rutter, Moffitt, and Caspi, “Gene-environment interplay and psychopathology,” p. 229.)
Individual genes and their environments interact to initiate a complex developmental process that determines adult personality. Most characteristic of this process is its interactivity: Subsequent environments to which the organism is exposed depend on earlier states, and each new environment changes the developmental trajectory, which affects future expression of genes, and so forth. Everything is interactive, in the sense that no arrows proceed uninterrupted from cause to effect; any individual gene or environmental event produces an effect only by interacting with other genes and environments. (Turkheimer, “Three laws of behavior genetics and what they mean,” p. 161.)
in truth human height has fluctuated dramatically over time.
This from height anthropologist Richard Steckel: “We have 1200 years of adult male height trends in Northern Europe that show that height was greatest in the early middle ages, when there was a warmer climate, and reached a minimum in the Little Ice Age of the 17th and 18th centuries.” (Steckel, “Height, Health, and Living Standards Conference Summary,” p. 13.)
Also: American and British teenagers were six inches taller, on average, than their predecessors a century earlier. (Ceci, Rosenblum, DeBruyn, and Lee, “A Bio-Ecological Model of Intellectual Development.”)
The New Yorker’s Burkhard Bilger: Bilger, “The Height Gap.”
A few more excerpts from Bilger’s piece:
Though climate still shapes musk oxen and giraffes—and a willowy Inuit is hard to find—its effect on industrialized people has almost disappeared. Swedes ought to be short and stocky, yet they’ve had good clothing and shelter for so long that they’re some of the tallest people in the world. Mexicans ought to be tall and slender. Yet they’re so often stunted by poor diet and diseases that we assume they were born to be small.
Biologists say that we achieve our stature in three spurts: the first in infancy, the second between the ages of six and eight, the last in adolescence. Any decent diet can send us sprouting at these ages, but take away any one of forty-five or fifty essential nutrients and the body stops growing. (“Iodine deficiency alone can knock off ten centimetres and fifteen I.Q. points,” one nutritionist told me.)
Steckel, after his work on slaves, went on to Union soldiers and Native Americans. (The men of the northern Cheyenne, he found, were the tallest people in the world in the late nineteenth century: well nourished on bison and berries, and wandering clear of disease on the high plains, they averaged nearly five feet ten.) Then he enlisted anthropologists to gather bone measurements dating back ten thousand years. In both Europe and the Americas, he discovered, humans grew shorter as their cities grew larger. The more people clustered together, the more pest-ridden and poorly fed they became. Heights also fell in synch with global temperatures, which reached a nadir during the Little Ice Age of the seventeenth century.
Around the time of the Civil War, Americans’ heights predictably decreased: Union soldiers dropped from sixty-eight to sixty-seven inches in the mid-eighteen-hundreds, and similar patterns held for West Point cadets, Amherst students, and free blacks in Maryland and Virginia. By the end of the nineteenth century, however, the country seemed set to regain its eminence. The economy was expanding at a dramatic rate, and public-hygiene campaigns were sweeping the cities clean at last: for the first time in American history, urbanites began to outgrow farmers.
In personal correspondence, Patrick Bateson warns: “[Don’t] overstate your case. Differences in genes can be correlated with a difference in behaviour or morphology. Not everyone will reach the same height if they are all given a superb diet. Pygmies, for example, produce less growth hormone or, in the case of other populations (the phenotype seems to have evolved at least five times in different parts of the world), are less receptive to growth hormone.”
“Maze-dull” rats, which had consistently tested poorly in those same mazes, making an average of 40 percent more mistakes.
This second group consistently stumbled through the same maze over and over again without remembering or learning, making an average of 40 percent more mistakes than the smarter group. They seemed obviously dumber than the Maze-bright strain, possessing an apparently inferior set of intelligence genes.
“a classic example of gene-environment interaction”: McClearn, “Genetics, Behavior and Aging,” p. 11.
temperature surrounding turtle and crocodile eggs determined their gender: Bateson, “Behavioral Development and Darwinian Evolution,” p. 52.
In 1972, Harvard biologist Richard Lewontin supplied a critical clarification that helped his colleagues understand GxE.
Paolo Vineis, chair of Environmental Epidemiology, Imperial College, London, explains:
This issue was clarified in an important paper by Richard Lewontin many years ago, but it is still a matter of confusion. The main idea of Lewontin’s paper is that when we evaluate gene-environment interactions we use the “analysis of variance” paradigm, that is, we try to combine the two main effects (genes versus environment), plus their interactive term, in a linear model. Causal models presuppose a linear combination of factors as the base line, variances are then computed and the role of the two main effects (or their interaction) is apportioned accordingly. But, Lewontin argues, the analysis-of-variance approach is misleading. There is no theoretical justification for the presumption of a linear explanation (this is done for the sake of simplicity but does not correspond to any reasonable biological reason). By contrast, all the experiments done with, for example, Arabidopsis (a plant) or Drosophila(based for example on radiation-induced mutations) show that mutations cause a change in what is called the “norm of reaction,” that is, the ability of the organism to react to different environmental conditions. The way in which the mutant strain will react, say, to different temperatures, is not predictable if the environmental conditions are not specified. Usually what happens is “canalization,” that is, under “normal” conditions there is a certain norm of reaction that is the same for the wild type and the mutants, whereas in changing environments the wild type and the mutant differ in the norm of reaction. What this suggests is that in at least some cases a nonlinear explanation is going to be required. In practical terms, it means that all attempts to explain disease on the basis of either the environment or genes (or their interaction) are in fact doomed to fail, because two organisms with different gene variants will have exactly the same response in a normal environment, and a totally different response in an abnormal environment. (Italics mine.) (Vineis, “Misuse of genetic data in environmental epidemiology,” pp. 164–65. The paper Vineis is referring to is Lewontin, “The analysis of variance and the analysis of causes.”)
“the way genes and environments interact dialectically to generate an organism’s appearance and behaviour”: Pigliucci, “Beyond nature and nurture,” pp. 20–22.
“the individual animal starts its life with the capacity to develop in a number of distinctly different ways”: Bateson and Martin, Design for a Life, pp. 102–3.
“Everything we have learned about molecular biology has shown that gene activity is regulated by the intracellular environment,” explains McGill’s Michael Meaney. He continues:
The intracellular environment is a function of the genetic make-up of the cell and the extracellular environment (e.g. hormones released by endocrine organs, cytokines from the immune system, neurotransmitters from neurons, nutrients derived from food) [which is] also influenced by the environment of the individual. Neurotransmitter and hormonal activity is profoundly influenced, for example, by social interactions, which lead to effects on gene activity. (Meaney, “Nature, nurture, and the disunity of knowledge,” p. 52.)
Your life is interacting with your genes.
If genes are merely the bricklayers, where’s the foreman? Where’s the architect?
Amazingly, there is no architect. Like ant colonies, galaxies, and other complex emergent systems, the human body is a dynamic assembly abiding by certain strict laws of science but not following any master set of instructions. The outcome is a function of the ingredients and the process.
The University of Virginia’s Eric Turkheimer explains it this way: “Individual genes and their environments interact to initiate a complex developmental process that determines adult personality. Most characteristic of this process is its interactivity. Subsequent environments to which the organism is exposed depend on earlier states, and each new environment changes the developmental trajectory, which affects future expression of genes, and so forth. Everything is interactive, in the sense that no arrows proceed uninterrupted from cause to effect; any individual gene or environmental event produces an effect only by interacting with other genes and environments.”
The point here is not to suggest that every person has exactly the same biological advantages or limits, or exactly the same potential. We clearly do not. But understanding each person’s true potential is not something we’ll ever be able to do from a genetic snapshot. Too many developmental factors matter too much. When it comes to complex traits like intelligence and talent, we need to drop casual use of the word “innate” and instead strive to understand as much as we can about the gene-influenced, environment-mediated process called human development.
While the scientific use of the word “innate” is still under intense discussion among biologists, it’s clear enough that its popular use to refer to fixed, built-in, predetermined causes of complex traits is simply no longer supportable. It has become obsolete.
Like the popular use of the word “genes,” it is a mere stand-in for things we don’t understand about how we become who we are, a shorthand for the rich and enigmatic incubator of temperament, inclinations, and abilities. (Turkheimer, “Three laws of behavior genetics and what they mean,” p. 161. Bateson and Mameli, “The innate and the acquired.”)
Dynamic development was one of the big ideas of the twentieth century, and remains so.
Without an infectious symbol like E = mc2 or a phrase like “nature versus nurture,” this idea has been difficult to introduce to the public; few even bothered to try. Several decades passed while this transformative idea languished in obscurity and was eclipsed by other, more enthralling genetic headlines about Dolly the sheep, the Human Genome Project, “criminal genes,” and so on.
It languishes still. Meanwhile, in classrooms and baby nurseries everywhere, the oppressive reign of the gene-gift paradigm continues.