Though the pursuit of happiness is listed as an inalienable right in the U.S. Declaration of Independence, achieving happiness has never been that easy. In recent years, happiness research has become a hotly debated topic in social science, especially over what people need to be satisfied in their lives. Although things such as a good income, steady employment, a strong family life, a good education, and good health have all been linked to life satisfaction, research has not shown all that strong a relationship. Part of the problem seems to be that happiness has a way of returning to what psychologists call a “set point” or “baseline” of happiness. Also known as the "hedonic treadmill", happiness seems to be as much about personality and genetic factors as it is about good things happening in your life.
But is it possible for things like life satisfaction and well-being to be shaped by genetics? While previous research has found that happiness can be inherited, linking that to specific genes has always been difficult. A new study published in The Journal of Neuroscience, Psychology and Economics looked at the link between happiness and genetics as well as identifying a possible candidate for a "happiness gene". Conducted by Jan-Emmanuel De Neve of the University College London and his colleagues, the study focused on 5-HTTLPR, a gene which has been linked to emotional problems such as depression and has been called “the depression gene” in popular news stories.
Also known as the serotonin transport protein, 5-HTTLPR is involved in transporting serotonin back into cells after the chemical message serotonin relays is completed. Since serotonin is an important neurotransmitter associated with reducing level of stress hormones in stressful situations, different genetic variations of 5-HTTLPR appear to be connected to mood disorders, including depression. Chemical stimulants such as “ecstasy”, cocaine, and prescription anti-depressants also work by targeting the 5-HTTLPR gene complex. Though happiness is likely not linked to a single gene such as 5-HTTLPR, it represented a good starting point to seeing if genetic factors can affect life satisfaction.
The study used a sample of identical and fraternal twins taken from the National Longitudinal Study of Adolescent Health (ADD Health) and the Framingham Heart Study. The ADD Health study is a comprehensive project following more than 20,000 adolescents all the way through to adulthood using interviews and surveys. ADD Health also identified a smaller sample of twins raised together and the data collected have been commonly used to study the importance of genetic factors. As part of the study, genetic information was collected looking at different genes, including different variations of 5-HTTLPR. The participants were also asked questions about life satisfaction and mood.
By focusing on identical and fraternal twins, De Neve and his colleagues were able to examine the different roles that heredity and upbringing can have in shaping life satisfaction. Since identical twins share 100% of their genes while fraternal twins only share 50%, finding a higher correlation between life satisfaction and 5-HTLLPR gene length for identical twins than fraternal twins was strong evidence that genetics played a potentially important role in happiness.
As for the question of exactly why this particular gene can have a powerful effect on mood, that calls for a better understanding of how serotonin works in the human brain. In their article, De Neve and his colleagues point out that research has already shown that serotonin is involved in activating specific parts of the brain linked to negative emotions, particularly the amygdala and the perigenual cingulate. The role of the 5-HTTLPR gene and its different variations in activating serotonin production in response to positive and negative emotions is one possible explanation for how psychiatric medication works to control depression and other related mental health problems. But recent research has also found that the 5-HTTLPR gene can also influence more positive emotions, including optimism.
De Neve and his colleagues are careful to point out that positive and negative emotions are not necessarily opposites. The absence of depression does not automatically mean that someone is happy or vice versa. Still, individuals with short 5-HTTLPR genes appear more vulnerable to depression, especially when dealing with stressful situations while having the long form of the gene seem to provide better protection. In the same way, having the long form of the 5-HTTLPR gene can lead to an increased tendency towards life satisfaction although that also depends on a person’s overall life situation. The article also describe several attempts at replicating these results with another ADD Health sample as well as an independent heart study which have been only partially successful.
In discussing their findings, De Neve and his colleagues stress that genetic factors are only one part of the puzzle as far as life satisfaction is concerned. Along with environmental factors, the human genome contains a vast array of different genes that could be contributing to personality and mood. There is likely no single “happiness” gene as such. Still, research has shown a strong correlation between “long” and “short” forms of the 5-HTTLPR gene and mood states such as optimism and depression. Combined with that, the current study suggests that genetic variation can account for as much as 33% of the overall variation in life satisfaction and happiness. Whether this relationship will be confirmed by future research and what this might mean in understanding how genetics and environment work together in shaping human behaviour is something that needs to be studied further.