Mood gene

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A single gene known as 5-HTTLPR plays a key role in determining whether you become happy or sad. British researchers have identified the gene that affects if we are cheery or gloomy. This gene determines how the neurotransmitter serotonin functions within the brain. Serotonin, a hormone, transmits chemical messages between nerve cells, and has been closely linked to mood. Several anti-depressant drugs regulate serotonin levels.


Why should I be aware of this?

A study conducted by a trio of researchers from the University of Essex in Britain published in Britain’s Proceedings of the Royal Society B, found that people with different variants were more or less drawn to or repelled by both distressing and pleasing situations. [1]

The study found that those who had the long variant of the 5-HTTLPR gene showed a marked avoidance of negative material alongside a vigilance for positive material. When presented with images categorized as negative designed to inspire fear or stress, erotic or pleasant ones, and neutral ones, respondents possessing the long variant of 5-HTTLPR gene automatically screened out the screened out the frightening images and paid attention to the positive pictures. [2]

All about mood gene

Scientists assumed for some time now that humans are constructed differently: adversity depresses some, but not others.

The effects of stressful events in early adulthood -- and the way people respond to them - are mediated by a single gene, called 5-HTT. The gene makes a protein that modifies nerve cells' use of serotonin, a chemical messenger important in the regulation of mood. The short version of the gene was linked (if weakly) to neuroticism.

On the other hand the long variant confers emotional resilience. A study in 2003, headed by behavioral geneticists from King's College, London, looked at developmental data on 847 New Zealanders who had been followed from ages 3 to 26. Stress did not produce depression on those who had two long genes. It made no difference whether the subjects had been mistreated severely in early childhood, nor whether they had later encountered deaths in the family, ill health or financial losses. But among those who possessed one or two short genes, adversity, whether early or recent, led to an increase in depression at age 26.


  • 70 percent of us have at least one short 5-HTT gene, and vulnerability to depression is normal. [3]
  • Most depression arises from an interaction of genes and experience. [3]
  • Chronic depression produces marked changes. Particular brain regions begin to shrink or show structural disorganization. Resilience factors -- perhaps including the protein produced by the 5-HTT gene -- mitigate that damage or allow for repair. [3]

90 degrees

The study is important as it throws light on the nature of depression, which public health campaigns call a disabling illness. But, often in society mood disorder is often not treated as an illness but a character trait. There is still a tendency among general practitioners under-treat depression. Whether depression should have full status as a physical disease in health insurance coverage or as a workplace disability remains a matter of public debate. [3]


Grapho-Therapy is particularly effective with children, because their handwriting (like their character) is in a formative stage. This makes it a perfect time to begin correcting undesirable traits and tendencies. But it is never too late, and even stubborn cases in adults will respond positively.


  • Happy or sad? Single gene controls mood
  • Tapping The Mood Gene


  1. Proceedings of the Royal Society B
  2. The Times of India
  3. 3.0 3.1 3.2 3.3 New York Times