Researchers now realise that some of what had been termed 'junk DNA' actually has important health functions

Anyone who's ever lost their car keys will know the annoying question: "Where did you have them last?" Knowing where to look is the real trick to routing them out. You'll never find them if you keep looking in the wrong place, however many times you check and recheck.

Speaking at the British Science Festival in Bradford on Wednesday, the biologist Dr Alasdair MacKenzie of the University of Aberdeen explained that researchers trying to fully understand how our DNA causes disease might not be looking in all the right parts of the genome.

"The sad news is that about 25-30% of us will suffer some horrible disease sometime in our live, for example, diabetes or heart disease, brought on by, for example, obesity. We're told that we are all susceptible because it's hard-wired into our genes – snippets of DNA within our genomes that encode proteins – the bricks and mortar of life," said MacKenzie.

The past decade of genetic studies has revealed that our 3bn-letter-long DNA code is more complex than anyone could have thought. The striking thing is that about 88% of disease-causing mutations are found outside of genes, in what MacKenzie called the "dark matter" of the genome. These areas were previously called "junk DNA" but researchers now realise that some of these are important parts of our cells with important functions. Certainly not junk.

"People are quite shocked by how little of the DNA creates protein," said MacKenzie. "98% of the whole genome is essential for a person's health."

MacKenzie's team has been specifically working to address the growing epidemic of obesity, a condition that is thought to be caused by an interplay between genes and environment in a ratio of about 70-30.

One of their results looks at the protein galanin, a regulator of appetite produced in the brain. An over-production of galanin not only affects the size of someone's appetite but it also influences people's choices. For example, someone may have a preference for fatty food or alcohol.

MacKenzie's team isolated a DNA fragment in the genome known as GAL5.1, which can be found in the non-coded part of the genome. They found that this bit of DNA acted as a switch that controlled the action of galanin – when it is active we get galanin. The switches tell the genes where, when and how much protein to produce.

In the future, scientists hope to develop new treatments which can use drugs to manipulate the activity of these switches. These designer drugs could potentially be used to treat all kinds of diseases.

Scientists are increasingly becoming interested in how mutations in human genomes, specifically the non-coded areas, affect these switches. With up to 88% of disease-causing mutations found in these non-gene areas, there seems to be plenty of opportunity for new discoveries.

With such attractive possibilities for tackling obesity, heart disease or depression, perhaps we should really be asking the question: "Are we there yet?"