A new study found that depression can make us physically older by speeding up the ageing process in our cells.
Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past.
These visible differences in a measure of cell ageing called telomere length couldn’t be explained by other factors, such as whether a person smoked.
The findings, in more than 2,000 people, appear in Molecular Psychiatry.
Experts already know that people with major depression are at increased risk of age-related diseases such as cancer, diabetes, obesity and heart disease.
This might be partly down to unhealthy lifestyle behaviors such as alcohol use and physical inactivity.
Depression can make us physically older by speeding up the ageing process in our cells
But scientists suspect depression takes its own toll on our cells.
To investigate, Josine Verhoeven from the VU University Medical Centre in the Netherlands, along with colleagues from the US, recruited 2,407 people to take part in the study.
More than one third of the volunteers were currently depressed, a third had experienced major depression in the past and the rest had never been depressed.
The volunteers were asked to give a blood sample for the researchers to analyze in the lab for signs of cellular ageing.
The researchers were looking for changes in structures deep inside cells called telomeres.
Telomeres cap the end of our chromosomes which house our DNA. Their job is to stop any unwanted loss of this vital genetic code. As cells divide, the telomeres get shorter and shorter. Measuring their length is a way of assessing cellular ageing.
People who were or had been depressed had much shorter telomeres than those who had never experienced depression. This difference was apparent even after lifestyle differences, such as heavy drinking and smoking, were taken into account.
Furthermore, the most severely and chronically depressed patients had the shortest telomeres.
Dr. Josine Verhoeven and colleagues speculate that shortened telomeres are a consequence of the body’s reaction to the distress depression causes.
“This large-scale study provides convincing evidence that depression is associated with several years of biological ageing, especially among those with the most severe and chronic symptoms,” they say.
However, it is unclear whether this ageing process is harmful and if it can be reversed.
British researchers have explained the way cancers make a chaotic mess of their genetic code in order to thrive.
Cancer cells can differ hugely within a tumor – it helps them develop ways to resist drugs and spread round the body.
A study in the journal Nature showed cells that used up their raw materials became “stressed” and made mistakes copying their genetic code.
Scientists said supplying the cancer with more fuel to grow may actually make it less dangerous.
Most normal cells in the human body contain 46 chromosomes, or bundles of genetic code. However, some cancerous cells can have more than 100 chromosomes.
And the pattern is inconsistent – pick a bunch of neighboring cells and they could each have different chromosome counts.
This diversity helps tumors adapt to become untreatable and colonize new parts of the body. Devising ways of preventing a cancer from becoming diverse is a growing field of research.
Scientists at the Cancer Research UK London Research Institute and the University College London Cancer Institute have been trying to crack how cancers become so diverse in the first place.
It had been thought that when a cancer cell split to create two new cells, the chromosomes were not split evenly between the two.
However, lead researcher Prof. Charles Swanton’s tests on bowel cancer showed “very little evidence” that was the case.
Instead the study showed the problem came from making copies of the cancer’s genetic code.
British researchers have explained the way cancers make a chaotic mess of their genetic code in order to thrive
Cancers are driven to make copies of themselves, however, if cancerous cells run out of the building blocks of their DNA they develop “DNA replication stress”.
The study showed the stress led to errors and tumor diversity.
Prof. Charles Swanton said: “It is like constructing a building without enough bricks or cement for the foundations.
“However, if you can provide the building blocks of DNA you can reduce the replication stress to limit the diversity in tumors, which could be therapeutic.”
He admitted that it “just seems wrong” that providing the fuel for a cancer to grow could be therapeutic.
However, he said this proved that replication stress was the problem and that new tools could be developed to tackle it.
Future studies will investigate whether the same stress causes diversity in other types of tumor.
The research team identified three genes often lost in diverse bowel cancer cells, which were critical for the cancer suffering from DNA replication stress. All were located on one region of chromosome 18.
