So, you’ve got your father’s blonde hair and you were raised in a cricket-mad household and you like cricket. But is it your genes or your childhood that’s responsible for your love of cricket or your thrill-seeking, or your obsession with spicy food?
Is it nature or is it nurture?
Everyone knows about the nature versus nurture debate — are we the products of the environment we grow up in, or are we the products of the genes we’re born with?
It’s one of the oldest questions in psychology, and it’s been intensely debated for more than a hundred years.
But current social research combined with the modern gene sequencing methods are reporting a third, more nuanced possibility: could the answer be both — nature and nurture?
Degrees of susceptibility
This third option is called the ’differential susceptibility hypothesis’ and it proposes that people can be sensitive or insensitive to the environment they grow up in depending on their genes.
It’s an intriguing idea — we all know people who are extraordinarily affected by bad circumstances, and others in similar circumstances who are affected very little.
But so far, the differential susceptibility hypothesis has not been very well researched.
This is because investigations have to start with very particular genes, and very particular questions about how these genes interact with environmental circumstances.
But a study published today in Translational Psychiatry has managed, against the odds, to do precisely that.
The study looks at variants in the improbably-named 5-HTTLPR — that is, different types of gene that make the protein which recycles serotonin in the brain.
Serotonin is the substance in the brain most involved with mood disorders, such as depression or anxiety.
Generally, there are two variants of this gene, ’short’ and ’long’. People who have two of the short version have previously shown associations with a higher incidence of a variety of mood disorders, slower responses to antidepressant medication and a variety of different sensitivities in their mental health.
But, as might be expected, this is hugely complicated. Other studies have showed no association between the prevalence of this gene and any problems with affective disorders.
So, what’s going on?
The long and short of it
In this study, three different groups of children had the nature of their 5-HTTLPR gene type determined and were examined on a standardised scale of positive affect — how frequently they report being interested, energetic, excited, lively, and so on.
In the first group, the parents rated themselves on a scale designed to measure positive parenting. In the second group, the children brought a parent into the laboratory, researchers observed the parent /child pair interacting, and rated the parent’s positivity. And in the third group, the children themselves were asked to rate their parents’ emotional warmth.
In all three scenarios, the results were the same — children with the short gene version showed a sensitivity to their emotional environment, and children with the long version didn’t.
That means children with the short gene pair who received less positive parenting reported less positive affect.
It also means that children in the same group (short gene) who received a positive and supportive environment reported more positive affect.
The sensitive (short gene) children were happier in the positive environment and sadder in the negative one.
They were sensitive to both positive and negative environments, while those in the long gene group were insensitive to both kinds of environments.
Scientists have long discussed the idea of a genetic vulnerability — a series of circumstances where genes and environment can interact badly, producing unwanted health outcomes, usually during childhood.
But this is one of the first good pieces of evidence for something more substantial again — a gene variation that seems to represent the presence of an overall sensitivity, not just a particular vulnerability.
Still, the evidence is just an association. The next step, of course, is to investigate this experimentally — to find a group of ’short gene’ children who are at risk, help their parents provide a more positive parenting style, and try to record an improvement in the children over time. (Obviously, there are ethical issues with researching the hypothesis other way around.)
Studies, such as this one, attempting to translate direct genetic evidence into ’real world’ outcomes are becoming increasingly more common as our ability to ask questions about genetic variations becomes more sophisticated.
The eventual outcome of this line of work may be better ways of taking care of people in the population who have specific vulnerabilities and whom we can identify before they develop problems. But it might be a while yet before we find a ’spicy food’ gene.