CONTROLLING changes in the structure of human chromosomes could hold the key to new ways to battle cancer and other chronic health conditions.

At the end of each of our 46 chromosomes is what is called a telomere, a loop-shaped structure that functions much like the plastic tip on shoelaces.

As we get older, the telomeres naturally get shorter and send out messages to our cells that they can stop dividing - an important factor in preventing cancer from developing.

However, some people are born with abnormally short telomeres, putting them at risk of bone marrow failure, pulmonary fibrosis and cancer.

Telomere shortness has also been linked to cardiovascular disease and diabetes.

Scientists have known for a long time that abnormally short telomeres are related to these chronic conditions, but they've been stumped about the underlying cause.

Now a team of Australian genetic researchers has discovered that it's changes to the loop structure of the telomeres that's to blame for making them abnormally short.

Dr Tony Cesare, of the Children's Medical Research Institute at Westmead in Sydney, says when the loop opens up, it exposes the end of the chromosome.

Nearby cells interpret that change as the telomere no longer being healthy and that they should stop dividing.

"We would predict what's happening is these loops are opening up at a young age and this is leading to tissue failure and causing disease," he told AAP.

Dr Cesare and his team also discovered that some chemotherapy drugs can cause the telomere loops to open and send signals to cells that it's time to "retire".

They want to now investigate if they can control the opening of the telomere loops. It may give doctors a valuable new tool in their battle against cancer.

"If we can promote that process and make that happen more efficiently in cancers, that would hopefully kill cancer cells," he said.

At the same time, being able to control the opening of the telomere loop could mean young people with genetic conditions may be less likely to develop chronic conditions.

"So we want to help protect the structure where necessary and help destabilise the structure when that would be beneficial," Dr Cesare said.

The next step for Dr Cesare and his team will be to understand how to stabilise the telomere loop structure as a way of preventing the onset of genetic diseases.

He first came up with the theory about telomere loops while studying for his PhD in 1999.

Thanks to recent advances in technology, he's been able to use super-resolution microscopes to see the loops in 10 times more detail than in the past.

Details of Dr Cesare's study of telomeres has been published by the journal Molecular Cell on Friday.