David was a classic dandelion child, living comfortably and happily despite his less than idyllic home life. Melissa, on the other hand, was an orchid, and the care and climate of her childhood failed to meet her high standards. Their respective dispositions had an enormous impact on the outcome of their lives, and beyond that, the lives of their children. Not only are Melissa’s children at a socioeconomic disadvantage, living in near poverty and raised by an emotionally immature mother with a drug problem, they also have a 50 percent chance of inheriting the genes responsible for causing high biological sensitivity to context. Among her several children, those who inherit low BSC genes may overcome their adverse circumstances, while those with high BSC have the odds stacked much higher against them. Exposed and susceptible to poor rearing environments, high BSC children will often continue the cycle of poverty and addiction, passing it down to their own children, and so on.
Melissa and David aren’t the only people in this situation. Millions of families like theirs will show similar patterns, where dandelion children soldier on despite emotional and financial setbacks, and orchid children flounder. And since people typically meet, befriend, and marry people in their own socioeconomic level, the genes for low and high BSC may begin, over many generations, to separate. And the same is true on the opposite end of the spectrum. Marcy — Melissa’s prosperous twin sister, who was adopted by a wealthy family — is able to offer her children a life of privilege, opportunity, and unwavering support. Though all of them have a great shot at doing well and succeeding in any career they choose, the ones with high BSC will be able to truly maximize their potential, much as Marcy herself did.
Thus, just because a majority of high BSC children live in adverse circumstances doesn’t mean the environment directly caused high BSC; generations of genetic susceptibility may have simply attracted the more high-reactive individuals to the far ends of the environmental spectrum.
However, our reluctance to endorse every aspect of Boyce’s model doesn’t mean we reject his theory outright. Quite the opposite. His claim that biological sensitivity to context is an adaptive trait, as opposed to a maladaptive one, is well-documented. Nor do we entirely reject the notion that BSC is environmentally determined. We simply think that these influences might have a slightly different origin than Boyce describes.
We’ve known for some time that nature and nurture aren’t diametrically opposed, and that the enmity between genetic determinists and behaviourists was little more than political posturing and a case of tunnel vision. Not only are the two factors entwined through the gene by environment interactions we’ve discussed so far, they are actually linked by an intricate network of molecules capable of brokering exchanges between them. How they do so forms the crux of an important and exciting new science called epigenetics.
Section 3
Let’s Talk About Stress, Baby
“We are running 21st century software, our knowledge,
on hardware that hasn’t been upgraded for 50,000 years,
and this lies at the core of many of our problems.”
— Ronald Wright
Chapter 8
The Genetic Fuse Box
Autumn 1944: The memory of D-Day burns like a righteous fire in the furnace of the American military, driving the troops on with renewed vigour. Allied forces have made comfortable advances into Western Europe, carving out swaths of mainland and gunning for the heart of the Third Reich. On the Eastern Front, the Soviet war machine trundles inexorably westward, fueled by an endless stream of soldiers and a slow-burning anger at Germany’s betrayal. Things look bad for the Axis. Their westernmost holding, the Netherlands, seems next in line to fall. The Dutch are mutinous and the Allies are closing in. In a fit of desperation and petulance, the Germans cut off the food supply to the western half of the Netherlands and flood the fields, ruining the remains of what was already a subpar crop. American attempts to ship in supplies by barge fail, as winter has set in early and the canals have frozen solid. The Dutch, sealed off on all fronts and left with dwindling food supplies, face the harshest famine in their recent history.
Wait. This sounds familiar, doesn’t it? We described the Dutch Hunger Winter in chapter 3. As you may recall, the effects of the famine did not dissipate in the spring, when the embargo was lifted and the canals unfroze. They reverberated throughout the generations, affecting the children and even the grandchildren of those who had experienced the famine firsthand. Women pregnant during the famine gave birth to children predisposed to heart disease, breast cancer, and obesity. And these conditions didn’t just appear randomly in the affected cohort. Each one correlated to a set of distinct variables, particularly the gender of the child and how far along they were in their gestation when food supplies hit their nadir.
When we first mentioned the Dutch Hunger Winter, it was to illustrate how the environment influences child development in a manner once considered the sole dominion of genes. But we didn’t tell you how the environment went about exerting this influence. We touched on some relatively crude mechanisms, such as how our surroundings provide the basic materials genes need to build their protein products — you may recall the example of hair colour being determined in part by the body’s supply of copper — and attachment theory covers the development of less tangible traits, such as personality or behaviours. But obesity and heart disease aren’t behavioural conditions accounted for by neural plasticity. Nor can the environment’s influence over them be explained away by simple molecular supply and demand. Something more complicated is at play here, something that accounted for environmental conditions (food scarcity) and instructed the fetus to adjust accordingly (store energy in fat cells at an above-average rate). This kind of complex physiological action is generally the purview of genes, but genes aren’t that proactive. They can’t deliberately adapt to abrupt changes in the environmental landscape — at least, not on their own. Perhaps the gene for nutritional thriftiness exists in all of us, but remains to varying degrees inactive, waiting for some outside influence to crank up production. That outside influence is what epigenetics is all about.
Spool and Thread
Picture a strand of DNA in your mind’s eye. Chances are you conjured up, without much effort, an image of two thin ribbons spiralling around one another in the famous double helix pattern, the twin strands connected at regular intervals by nucleotide bonds like rungs on a twisted ladder. This picture is not fundamentally wrong, but it lacks some key details. When not being transcribed, DNA wraps itself around proteins called histones, which cluster tightly together in groups of eight called nucleosomes. Nucleosomes congregate in a squat, highly dense material called chromatin, which, as its name suggests, forms chromosomes.
Think of histones as spools and DNA as the string wound around them. Without these genetic spools, DNA would drift through our cells like giant hairballs, bulgy and tangled and constantly snagging on every protruding protein edge, leaving our genes tattered and ripe for mutation. Histones keep our DNA organized and protected. They also help control the frequency at which our genes code.[27]
When a gene is ready to be transcribed, its portion of DNA unravels itself from the histone, allowing access to the double helix strand. At all other times, our DNA remains neatly wrapped around its histone spools. By adjusting their grip, so to speak, on the DNA spooled around them, histones control how often the genes it protects are available for transcription. And the tightness of their grip is determined by a loose array of proteins and molecules called epigenetic tags.[28]
Nor are histones the only part of our chromosomes controlled by epigenetics. Various molecular hangers-on festoon the