Stressed girls with a family history of depression may age faster than girls without a family history of the illness. This is according to a new study published in the journal Molecular Psychiatry.
Numerous studies have suggested a link between stress, depression and physical changes in the body. Specifically, studies have linked stress to increased risk of depression, and depression to premature aging, determined by shortened telomere length.
Telomeres are structures at the end of chromosomes that protect them from deterioration. Telomeres shorten in length as we age, although oxidative stress and other DNA-damaging processes can cause them to shrink.
According to the research team – including Ian Gotlib of Stanford University in California – it has been unclear as to what comes first: stress, depression or reduced telomere length.
With the aim of finding out, the team analyzed 97 girls aged 10-14 years who were free of depression but who were at high risk of depression due to a family history of the illness.
“Studying such a population is critical in assessing whether shortened telomere length is a pre-existing condition or risk factor for developing depression, or, alternatively, is a response to, or concomitant of, major depressive episodes,” the researchers say.
Gotlib and colleagues assessed the telomere length of these girls by analyzing DNA samples and compared them with the telomere lengths of age-matched girls who had no family history of depression.
All participants underwent stress tests and were interviewed about stressful situations they had experienced. Their cortisol levels – a hormone produced in responses to stress – were measured before and after the stress tests.
The researchers found that 12-year-old girls at high risk of depression had shorter telomere lengths – equivalent to 6 years of biological aging in adults – compared with girls without a family history of depression.
Gotlib says he was surprised by the findings. “I did not think that these girls would have shorter telomeres than their low-risk counterparts – they’re too young,” he adds.
Commenting on their findings, the team says:
“The results of this study indicate that healthy children at familial risk for depression have shorter telomeres than do their non-risk peers. Thus, telomere shortening appears to be an antecedent to, and potentially a risk factor for, the onset of depression.”
Furthermore, the researchers found that girls with shortened telomere length had higher cortisol reactivity in response to stress.
Overall, the team’s findings suggest that girls at high-risk of depression are more likely to have shorter telomere length and that stress may mediate this effect.
The researchers say these findings are worrying, as telomere shortening in this population has important implications for health. They explain:
“Telomere shortening is not only a marker of stress, but is also a mechanism of biological aging. Insufficient telomere maintenance can accelerate biological aging and increase individuals’ risk for experiencing age-related chronic diseases.”
As such, the team says it is important that individuals who are vulnerable to telomere shortening, such as those at high risk of depression, are identified. “Also,” they add, “it is important to follow these girls longitudinally to examine whether telomere length influences the onset of major depressive disorder and whether developing depression, in turn, contributes to further shortening of telomeres.”
Gotlib and colleagues say it may be beneficial for young girls with a family history of depression to learn stress-reduction techniques, such as attention bias training – where an individual learns to focus on the positive areas of life rather than the negative.
Furthermore, they note that exercise has been shown to delay telomere shortening in adults, so this may be an option for girls at high risk of depression.
Medical News Today recently reported on a study by researchers from the University of California-Los Angeles, in which they claim to have discovered a gene that could slow the aging process when activated in key organs, such as the brain and intestines.