The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (4 page)

When it comes to more complex traits like physical coordination, personality, and verbal intelligence, gene-environment interaction inevitably moves the process even further away from simple Mendelian patterns.

What about single genetic mutations that predictably cause diseases such as Huntington’s disease?

Single-gene diseases do exist and account for roughly 5 percent of the total disease burden in developed countries
. But it’s important not to let such diseases give the wrong impression about how healthy genes work.
“A disconnected wire can cause a car to break down
,” explains Patrick Bateson. “But this does not mean that the wire by itself is responsible for making the car move.” Similarly, a genetic defect causing a series of problems does not mean that the healthy version of that gene is single-handedly responsible for normal function.

Helping the public understand gene-environment interaction is a particular burden, because it is so enormously complex. It will never have the same easy, snap-your-fingers resonance that our old (misleading) understanding of genes had for us. Given that, the interactionists are lucky to have Patrick Bateson on their side. A former biological secretary to the Royal Society of London and one of the world’s leading public educators about heredity, Bateson also carries a powerful symbolic message with his surname. It was his grandfather’s famous cousin, William Bateson, who, a century ago, first coined the word “genetics” and helped popularize the earlier, simpler notion of genes as self-contained information packets that directly produce traits. Now the third-generation Bateson is helping to significantly update that public understanding.

“Genes store information coding for the amino acid sequences of proteins,” explains Bateson
. “That is all. They do not code for parts of the nervous system and they certainly do not code for particular behavior patterns.”

His point is that genes are several steps removed from the process of trait formation. If someone is shot dead with a Smith & Wesson handgun, no one would accuse the guy running the blast furnace that transformed the iron ore into pig iron—which was subsequently transformed into steel and later poured into various molds before being assembled into a Smith & Wesson handgun—of murder. Similarly, no gene has explicit authorship of good or bad vision, long or short legs, or affable or difficult personality. Rather, genes play a crucial role throughout the process. Their information is translated by other actors in the cell and influenced by a wide variety of other signals coming from outside the cell. Certain types of proteins are then formed, which become other cells and tissues and ultimately make us who we are. The step-by-step distance between a gene and a trait will depend on the complexity of the trait. The more complex the trait, the farther any one gene is from direct instruction. This process continues throughout one’s entire life.

Height can provide a terrific insight into the gene-environment dynamic. Most of us think of height as being more or less directly genetically determined. The reality is so much more interesting.
One of the most striking early hints of the new understanding of development as a dynamic process emerged in 1957
when Stanford School of Medicine researcher William Walter Greulich measured the
heights of Japanese children
raised in California and compared them to the heights of Japanese children raised in Japan during the same time period. The California-raised kids, with significantly better nourishment and medical care, grew an astonishing five inches taller on average. Same gene pool, different environment—radically different stature.
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.

It turns out that a wide variety of environmental elements will affect the genetic expression of height: a single case of diarrhea or measles, for example, or deficiencies in any one of dozens of nutrients. In Western cultures of the twenty-first century, we tend to assume a natural evolutionary trend of increased height with each generation, but
in truth human height has fluctuated dramatically over time
in specific response to changes in diet, climate, and disease. Most surprising of all, height experts have determined that, biologically, very few ethnic groups are truly destined to be taller or smaller than other groups. While this general rule has some exceptions, “by and large,” sums up
The
New Yorker
’s Burkhard Bilger
, “any population can grow as tall as any other … 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.”

Born to be small. Born to be smart. Born to play music. Born to play basketball
. It’s a seductive assumption, one that we’ve all made. But when one looks behind the genetic curtain, it most often turns out not to be true.

Another stunning example of the gene-environment interactive dynamic arrived, coincidentally, just one year after Greulich’s Japanese height study. In the winter of 1958, Rod Cooper and John Zubek, two young research psychologists at the University of Manitoba, devised what they thought was a classic nature/nurture experiment about rat intelligence. They started with newborn rat pups from two distinct genetic strains: “Maze-bright” rats, which had consistently tested well in mazes over many generations, and
“Maze-dull” rats, which had consistently tested poorly in those same mazes, making an average of 40 percent more mistakes
.

Then they raised each of these two genetic strains in three very different living conditions:

Enriched environment:
featuring walls painted in rich, bright patterns and many stimulating toys: ramps, mirrors, swings, slides, bells, etc.

Normal environment:
with ordinary walls and a moderate amount of exercise and sensory toys.

Restricted environment:
essentially rat slums with nothing but a food box and a water pan; no toys or anything else to stimulate their bodies or minds.

In broad terms, it seemed easy enough to predict the outcome: each strain of rat would get a little smarter when raised in the enriched environment and get a little dumber when raised in the poor environment. They expected to have a graph that looked something like this:

Courtesy of Hadel Studio

Instead, the results looked like this:

Courtesy of Hadel Studio

The final data were quite shocking. Under normal conditions, the Maze-bright rats had consistently outperformed the Maze-dull rats. But in both extreme environments, they performed virtually the same. The Maze-bright rats raised in the restricted environment made almost exactly the same number of mistakes as the Maze-dull rats raised in the restricted environment (point A, above). In other words, when raised in an impoverished environment, all the rats seemed equally dumb. Their “genetic” differences disappeared.

The same thing happened with the enriched environment. Here, the Maze-bright rats also made very close to the same number of mistakes as the Maze-dull rats (point B, above—the difference was deemed statistically insignificant). Raised in an exciting, provocative environment, all the rats seemed equally smart. Again, their “genetic” differences disappeared.

At the time, Cooper and Zubek didn’t really know what to make of it. The truth was that these original “genetic” differences hadn’t really ever been purely genetic. Rather, they had been a function of each strain’s GxE development within its original environment. Now, when developing within different environments, each strain was producing very different results. And in the case of both the enriched and restricted environments, the different genetic strains turned out to be a lot more alike than they had previously seemed.

In the decades that followed, the Cooper-Zubek study emerged as
“a classic example of gene-environment interaction
,” according to Penn State developmental geneticist Gerald McClearn. Many other scientists agree.

Over this same time period, hundreds of examples emerged that gradually forced a wholesale rethinking of how genes operate. Almost in disbelief, biologists observed that

• the
  temperature surrounding turtle and crocodile eggs determined their gender
  

• young, yellow-skinned grasshoppers became permanently black skinned for camouflage if exposed to a blackened (burnt) environment at a certain age
  

• locusts living in a crowded environment developed vastly more musculature (suitable for migration) than locusts living in less crowded conditions
  

In these and so many other instances, environment A seemed to produce one kind of creature while environment B produced another creature entirely. This level of trait modification was simply impossible to comprehend under the old G+E idea that genes directly determined traits. The new facts demanded a whole new explanation of how genes function.

In 1972, Harvard biologist Richard Lewontin supplied a critical clarification that helped his colleagues understand GxE
. The old nature-and-nurture view featured a one-way, additive sequence like this:

Genes trigger the production of proteins, which guide the functions of cells, which, with some input from the outside world, form traits.

The new GxE was a much more dynamic process, with every input at every level influencing every other input: