In honor of the 4th of July and in the spirit of the Declaration of Independence, The Atlantic published a nice piece on the “Pursuit of Happiness” this week, specifically on how our community and environment can shape our mood and mindset, and how local governments are initiating public service projects to aid in our psychological well-being. However, a study published in the Journal of Human Genetics last month by behavioral economists at the London School of Economics suggests that it is not external factors but rather our genes and neurotransmitters (most notably serotonin) that determine how happy we are.
Serotonin has been linked to happiness and empathy, and a depletion of it is often seen in patients with depression. Many common antidepressants work by elevating levels of serotonin in the brain, including SSRIs (selective serotonin reuptake inhibitors), the most commonly prescribed medication for depression, which prevents the retraction of serotonin back into the cell after it has been released. This recycling of serotonin occurs naturally in the brain, with neurotransmitter transporters binding to the chemical in the synapse, taking the serotonin back up into the cell, and enabling it to be released again. The serotonin transporter gene 5-HTT is involved in the expression of the proteins that form these transporters and has two different forms it can take, a long or a short version. The long allele of 5-HTT results in more transporters being expressed, however, paradoxically, researchers have recently discovered that individuals who carry two long versions of the gene are significantly more likely to report higher levels of subjective well-being than those who inherited two short versions of the allele. In the study by Dr. Jan-Emmanuel De Neve, 69% of those with the long versions rated themselves as either satisfied or very satisfied with their lives, as opposed to only 38% of people with the short versions. While this is contradictory to the theory behind SSRIs, which prevent the recycling of the neurochemical and thus enable higher levels of serotonin to be present in the synapses, the greater number of transporters in the long allele population permits faster turn-over, facilitating greater release and higher, more stable levels in the brain.
On the other end of the spectrum, individuals with short alleles are known to have decreased brain density in the amygdala and limbic circuitry, areas implicated in emotion regulation and fear responses, impairing their perception and reaction to emotional stimuli. Those with short alleles have a higher risk of depression, although this association is somewhat tenuous as the 5-HTT gene directly only accounts for 10% of an individual’s susceptibility to anxiety or depression. Most likely, it is a gene-environment interaction that determines an individual’s likelihood of developing depression, as individuals with short alleles are more prone to react poorly or with greater anxiety to bad news.
Thus, returning to The Atlantic article, to what extent can our environment really foster a positive affect, and do things like city planning–improving traffic flow or building green spaces–really influence our overall levels of happiness? How much do the little things in our environment matter? Sure it’s unpleasant to sit in traffic and much more agreeable to eat lunch under a tree, but in the greater manifestation of mood do these things affect us on such a fundamental level? After the immediate physical or aesthetic enjoyment, are there pervasive lingering effects? Surely it is more the people we surround ourselves with and our own internal perception of events that determines our mood. How much of an effect do we have on our own happiness and how much is determined by our surroundings? What truly makes us happy?
Brain Study 