A Genetically Mediated Bias in Decision Making Driven by Failure of Amygdala Control:
Genetic variation at the serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with altered amygdala reactivity and lack of prefrontal regulatory control. Similar regions mediate decision-making biases driven by contextual cues and ambiguity, for example the "framing effect." We hypothesized that individuals hemozygous for the short (s) allele at the 5-HTTLPR would be more susceptible to framing. Participants, selected as homozygous for either the long (la) or s allele, performed a decision-making task where they made choices between receiving an amount of money for certain and taking a gamble. A strong bias was evident toward choosing the certain option when the option was phrased in terms of gains and toward gambling when the decision was phrased in terms of losses (the frame effect). Critically, this bias was significantly greater in the ss group compared with the lala group. In simultaneously acquired functional magnetic resonance imaging data, the ss group showed greater amygdala during choices made in accord, compared with those made counter to the frame, an effect not seen in the lala group. These differences were also mirrored by differences in anterior cingulate-amygdala coupling between the genotype groups during decision making. Specifically, lala participants showed increased coupling during choices made counter to, relative to those made in accord with, the frame, with no such effect evident in ss participants. These data suggest that genetically mediated differences in prefrontal–amygdala interactions underpin interindividual differences in economic decision making.
Check out the Wikipedia entry on
5-HTTLPR; lots of behavioral phenotypes associated with this variant.
ScienceDaily:
The researchers also measured the degree of interaction, or connectivity, between the amygdala and the prefrontal cortex, the brain region most implicated in human intelligence, personality and decision making. When resisting the frame effect, the participants with two copies of the long variant had stronger connectivity between the prefrontal cortex and amygdala, while those with a pair of short variants did not.
"This difference in connectivity is really interesting," says Dr Roiser. "It suggests that the volunteers carrying the long variant might regulate automatic emotional responses, which are driven by the amygdala, more efficiently, lessening their vulnerability to the framing effect.
"This one gene cannot tell the whole story, however, as it only explains about ten per cent of the variability in susceptibility to the framing effect. What determines the other ninety per cent of variability is unclear. It is probably a mixture of people's life experience and other genetic influences.
"An interesting question would be whether the gene might affect real-life decision-making. For example, traders in banks need to make quick and accurate estimations of risk and consistent decisions, no matter how the information is presented to them. So you might hypothesise that traders with the long genetic variant would make more consistent decisions, though this needs to be tested in future research."
So this genetic variation only explains 10% of the variation within the population when it comes to frame effect in behavioral economics. Fair enough. But, I do wonder if in the current political environment fewer would oppose genetically black-balling individuals with the short variants of 5-HTTLPR from becoming traders! (I'm not proposing this seriously myself, but I think there might be some amygdala-driven acceptance of this sort of genetic profiling right now even if the returns are small)
Labels: Behavioral Economics, Economics, Neuroscience
