Family and Parenting 3-Book Bundle. Michael Reist
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Conceivably, then, if Amelia’s father played a variety of music around the house during her gestation, she would have become familiar with the notions of melody, harmony, and counterpoint before she had even drawn her first breath. This is not to say she would have been composing symphonies in her crib, but repeated listening would have attuned her ear to the pitches and intervals common in Western music. Perhaps just as importantly, she would have developed a positive association with the songs she heard in utero, making it that much more likely she would take to music as a child.
As Amelia grew, her musical upbringing would have continued to influence her behaviour. There would have been musical scores lying around for her to ponder, tapes and CDs for her to listen to, and instruments for her to tinker with. And even if her father was not the type of man to force his child to follow in his footsteps, he would almost certainly have encouraged any interest in music that Amelia displayed. After all, what parent wouldn’t want their child to feel passionate about the same things they do?
We inherit more from our parents than our chromosomes. They are the ones who teach us, feed us, scold us when we misbehave, and console us when we scrape our knees or embarrass ourselves at school. They are responsible for cultivating the environments in which we are raised. We are as much the beneficiaries of their affluence (or lack thereof), their dispositions, and their teachings as we are of their genes.
Of course, none of Amelia’s hypothetical early training can guarantee that she will become a musical prodigy. Innate ability does exist, and there are limits to the extent that environmental factors can sculpt an individual. They can chisel out a form, but the genetic material from which the subject is carved will inevitably factor into the final outcome of the sculpture. What’s more, unlike a sculpture, humans are not passive subjects prostrate before the whims of their environment. They have the power to change their surroundings, either through the ingenuity of invention or by simply deciding to live in, speak to, and engage with the places, people, and pursuits that most interest them. A child’s natural talents influence his behaviour, which in turn influences the environmental factors he will encounter. Children generally like to do what they’re good at, and the more they do it, the better at it they get. It is in these instances where the nature versus nurture divide seems truly absurd. Without an inherent knack for music or chess or skateboarding, a child will be less inclined to dedicate the time necessary to improve, but if they never dedicate the time in the first place, they won’t improve no matter how innately talented they are.
Chapter 3
The Usual Suspects
It’s after midnight. The investigators hunker over a desk loaded with papers, coffee mugs, and stacks of manila folders. Their eyes, red and stinging from the room’s fluorescent lights and the lateness of the hour, pore over the contents of a folder labelled “7-repeat,” a member of the prominent DRD4 family with a nasty reputation. It’s a repeat offender, convicted on charges of aggravated ADHD and second-degree substance dependence. One of the investigators points to a line in the report. The other jots down the info in a notepad. Their efforts haven’t been in vain. They can pin the suspect to 18 victims in their sample alone.
They parse the data, make sure there isn’t some variable skulking behind the scenes, setting 7-repeat up as a fall guy. Nothing turns up. The case looks promising. With a satisfied nod, the investigators write up a warrant for further scrutiny. The charge: aiding and abetting the development of depression in susceptible children. A serious offence.
The human genome is a vast and labyrinthine network of codependent variables, dozens of which can be responsible for a single, seemingly simple trait. Nevertheless, researchers studying the effects of gene-by-environment interactions on childhood development seem to come across the same few subjects over and over again. These “usual suspects” are not the sole focus of this book — we will discuss other genes as well, along with studies that don’t focus on any one gene in particular — but their names will be mentioned frequently over the following chapters, so it is perhaps worth getting to know them. However, before we do that, we should first take a moment to discuss what exactly a gene is.
What Is a Gene?
It is outside the scope of this book to chronicle every gene responsible for moderating a person’s susceptibility to adverse conditions. Such a list would be far too extensive for our purposes, nor could its contents be truly exhaustive. The human genome contains a complex interplay of genetic and epigenetic variables (more on epigenetics in a later chapter), and our understanding of how it works is still far from comprehensive. The common notion that one gene is responsible for one trait is at best overly simplistic, and at worst completely false. Even the most simplistic traits are determined by multiple genes, and a single gene can be responsible for multiple traits.[7]
Perhaps part of the problem stems from the word gene itself. Despite the fact that just about everyone has heard of them, few people could accurately tell you exactly what genes are. This confusion extends into the scientific community, where the precise definition of the word gene remains fluid, as new discoveries continue to roil the already murky waters of our understanding. You might be wondering how this could be. We’ve cloned cats and sheep. We’ve made great strides in the field of genetic therapy. We’ve mapped the human genome. How could we have done all that without even knowing what a gene is?
The reason is that genes are more of a theoretical construction than a physical thing. They are a method of categorizing data in a manner satisfying to the human mind. But they do not, strictly speaking, exist.
When we discuss DNA, the molecules that make up the abstract concepts we refer to as genes, we are on firmer ground. The essential buildings blocks of genetics are nucleotides, tiny molecules comprised of a sugar, a phosphate, and a nucleobase. The bases determine the character of the nucleotide. They come in four varieties: adenine, thymine, cytosine, and guanine. Nucleotides are commonly referred to by whatever base they possess or, when documented in sequence, by each base’s first initial (A, T, C, and G, respectively).
The sugar of one nucleotide bonds readily with the phosphate of another, allowing nucleotides to form chains millions of units long called polymers. Each polymer links up with a sympathetic partner running parallel, and together the two molecules entwine, forming the iconic double helix as depicted on the front of biology textbooks the world over. Unlike the sugar–phosphate bonds of each individual polymer, which can occur regardless of which bases the adjacent nucleotides possess, the bonds between the two polymers are highly specific. Each nucleotide has only one compatible molecule: adenine links with thymine, and cytosine with guanine. As a result, each polymer forms a perfect template for its partner — by observing the nucleotide sequence of one strand, one could assemble a flawless replica of the other. This attribute is the backbone of genetic inheritance.
Nucleotides are the letters with which the sweeping epic of the human genome is written, and their alphabet, at a mere four characters, is mercifully small. However, just as an Anglophone could not pick up a book written in Swedish and read it simply by identifying the consonants and vowels, understanding the alphabet of DNA means little without an adequate grasp of its lexicon and grammar.
The nucleotide letters form “words” called codons, which in the language of DNA are all three letters long. Each codon represents an amino acid. When placed in sequence, they instruct the cells they inhabit to construct a series of amino acids called a polypeptide chain. The beginning and end of each chain is determined by special “start” and “stop” codons. These codons