The genetic perspective - Nature or nurture?

Anxiety: A Very Short Introduction - Daniel Freeman, Jason Freeman 2012

The genetic perspective
Nature or nurture?

’Murder, like talent, seems occasionally to run in families’, quipped the Victorian writer G. H. Lewes. Had he been discussing anxiety, Lewes could have allowed himself a little more certainty. Anxiety really does appear to run in families. For example, a person prone to severe anxiety is likely to have a parent — and even a grandparent — with the same problem.

Why is this so? Do we inherit anxiety through our genes, or learn it from those closest to us? Are anxiety levels biologically hard-wired, or the product of life experiences (that is, our ’environment’)? Over the years, both explanations have been proposed by scientists. In this chapter, we’ll take a look at the evidence and try to answer that perennial question: is it nature or nurture?

Everyone is familiar with the term ’gene’, and most people are aware that genes are involved in the transmission of characteristics from parent to child. Beyond this, however, we may be a little hazy! So what exactly are genes?

Every cell in our body contains 23 pairs of chromosomes, which are structures composed of deoxyribonucleic acid (DNA) and other biochemicals. One of each pair is inherited from our mother and the other from our father. Each chromosome, in every cell, contains thousands of genes — essentially extended molecules of DNA — which contain the biological rules that underlie our development. With the exception of identical twins, everyone’s genetic make-up is different.

How can we tell whether genes are responsible for anxiety (or indeed anything else)? A reasonable starting point is family history. However, although this strategy may highlight a similarity between family members, it doesn’t help us decide whether that similarity (or family aggregation) is the result of genes or environment. After all, families typically share a significant portion of both.

That said, certain types of families provide scientists with an important means of unravelling the gene/environment knot. These families are those that contain twins. Fraternal twins develop from separate eggs (hence the technical term ’dizygotic’) that have been fertilized by different sperm. Like all siblings, fraternal twins share 50% of their genes. Identical (or monozygotic) twins, on the other hand, result from the fertilization by a single sperm of one egg that subsequently splits into two. As a result, their genetic make-up is exactly the same. If an anxiety disorder, for instance, is more likely to be shared by identical twins than fraternal twins, we can be fairly certain that the difference is the result of genetic factors.

Fairly certain, but not definite because identical twins may have more experiences in common than fraternal twins (although in fact the assumption that the influence of environmental factors is equal for both types of twins seems to hold). Here’s where adoption studies come in. Imagine, for example, that identical twins have been separated at birth and placed with different adoptive families. (Clearly this isn’t an everyday occurrence; nonetheless, it does happen, and it has been studied by behavioural geneticists.)

Each twin is brought up with adoptive siblings. Yet, despite sharing the same family environment throughout their childhood, when tested as adults, the twin and his or her adoptive siblings have very different levels of anxiety. There is, though, a significant correlation between the score of one twin and the other, despite the fact that they have never met, and between the scores of the twins and their birth parents. (Between the anxiety levels of the twins and their adoptive parents, there’s no correlation.) Twin adoption studies of this type provide persuasive evidence of genetic influence, but they’re difficult to run, not least because identical twins are relatively scarce.

In the case of anxiety, research indicates that genes certainly play a role. Everyone feels anxious from time to time; we’d hardly be human if we didn’t. But just how frequently, how intensely, and how lastingly we become anxious is part of our personality. Psychologists call this predisposition to anxiety ’neuroticism’, and we all have a greater or lesser degree of it. Heritability for neuroticism has been put at around 40%. Anxiety disorders are moderately heritable — that’s to say, somewhere in the region of 20% to 40%. Research has also shown that some of the styles of thinking typical of people with anxiety problems — for example, the tendency to interpret ambiguous events as potentially dangerous or an acute sensitivity to the physiological changes triggered by anxiety — are also moderately heritable.

It’s important to be clear about the meaning of the term ’heritability’. What it doesn’t mean is that 40% of a person’s level of neuroticism is necessarily the result of their genes. What it signifies is that around 40% of the differences in levels of neuroticism across the population are likely to be genetic in origin. So heritability tells us nothing about individual cases; it’s relevant only to broad statistical samples. The remainder of the differences between people are the product of environmental factors.

Our genes clearly play an important role in determining our level of anxiety. But which genes are involved? The short answer is that scientists don’t yet know. Several candidates have been suggested: variants in the glutamic decaroxylase 1 gene (GAD1), for example, have been associated with general emotional disorders, including anxiety problems. This is intriguing because GAD1 is involved in the production and transmission of gamma aminobutyric acid (GABA), which, as we saw in Chapter 2, helps calm us down when we’re anxious. If GAD1 isn’t functioning correctly, then neither will GABA, leading to exaggeratedly high levels of anxiety.

The best genetic research on anxiety looks for a gene that, like GAD1, could lead to a physiological hypersensitivity to potential danger. But, despite many exciting leads, no single ’anxiety’ gene has been convincingly identified. To be meaningful, genetic studies require large numbers of people to be tested, huge amounts of research effort, and significant amounts of funding. Unsurprisingly, therefore, they are few and far between. And the findings from genetic studies are notoriously difficult to replicate: all too frequently, one research team will identify a plausible candidate gene only for subsequent studies to fail to find any link with anxiety.

Moreover, it seems unlikely that an experience as complex and varied as anxiety is the product of one or even a few isolated genes. Much more probable is the polygenic theory: that many different genes, each making a relatively small contribution, are involved in the generation and maintenance of anxiety. And so far the evidence suggests that what these genes are responsible for is a general tendency towards a high level of anxiety, or even general emotional arousal, rather than a specific anxiety disorder.

Identifying multiple genes involved in a complex interaction is clearly a tough assignment. But even if scientists are eventually successful, it may not be that those genes alone cause anxiety. Over the last decade or so, researchers have begun to see that there is a complex interaction of genes and environment. So, for example, although a person may be genetically susceptible to anxiety problems, they are by no means guaranteed to develop a disorder. That will happen only if the genetic vulnerability is triggered by particular life experiences. Equally, another person might experience the same events but, lacking the genetic vulnerability, will not go on to develop an anxiety disorder. As Avshalom Caspi and Terrie Moffitt have written:

the gene—environment interaction approach assumes that environmental pathogens cause disorder, and that genes influence susceptibility to pathogens.

Let’s look now at the ’environmental pathogens’ involved in anxiety problems.