Telomere shortening also was associated with higher levels of inflammation and oxidative stress in patients, both linked to cell damage and premature aging. Oxidative stress is an imbalance between destructive "free radical" molecules and the body's ability to neutralize them with antioxidants. The authors suggest that telomere shortening in very chronic depression may reflect an individual's cumulative exposure to biochemical stressors that promote cell death and increase the likelihood of physical disease.
"While this finding itself might seem depressing, there is yet good news: many lifestyle factors like exercise and aspects of diet have been linked to longer telomeres," said co-author Elissa Epel, PhD, an associate professor in the UCSF Department of Psychiatry. "So while our personal history matters, it is possible that what we do today may matter even more, in terms of protecting our telomeres."
Epel and co-author Elizabeth Blackburn, PhD, UCSF professor of biochemistry and biophysics, pioneered research on the impact of psychological stress on several biological markers of cell aging. Blackburn shared the 2009 Nobel Prize in Physiology or Medicine for her telomere research and co-discovery of the cellular enzyme telomerase. Telomerase helps repair and restore telomeres, protecting cells from damage related to premature aging.
In related work, the research team recently reported in the journal Molecular Psychiatry, available here, that individuals with MDD show increased activity of the telomerase enzyme. Depressed individuals with the lowest telomerase activity before antidepressant treatment, and those with the greate
|Contact: Kate Vidinsky|
University of California - San Francisco