As if major depressive disorder (MDD) didn’t already give people enough cause to abandon their sense of optimism, a new study into cellular aging has found links between depression and a greater risk for aging-related diseases, such as heart disease, diabetes, obesity, and cancer, suggesting to researchers that forms of depression could underlie cellular aging.
Cellular aging takes place as a result of several factors, but one of the more popular theories of aging deals with shortening telomeres. Think of telomeres as the plastic tips on the ends of shoelaces, but for chromosomes. Telomeres prevent the chromosome’s frayed ends from fusing together and tarnishing the cell’s blueprint. When a cell divides, the telomeres necessarily shorten in order to make up for the DNA that was lost in duplication. Scientists measure telomere length in base pairs — essentially DNA building blocks — with newborns having roughly 8,000 base pairs compared to a 65-year-old’s 1,500 base pairs.
According to the present study, published in Molecular Psychiatry, people suffering from MDD had significantly fewer base pairs than non-sufferers. Worse, the severity and duration of a person’s depression correlated highly with having shorter telomeres, even after researchers controlled for lifestyle factors, such as smoking, alcohol consumption, weight, and other factors known to accelerate cellular aging.
"Psychological distress, as experienced by depressed persons, has a large, detrimental impact on the 'wear and tear' of a person's body, resulting in accelerated biological aging," study author Josine Verhoeven, a researcher at the Free University in Amsterdam, told Live Science. Verhoeven and her team observed that many of these physical ailments also arise most often as people age, encouraging them that "the findings might help explain the variety of health complaints often experienced by people with major depression.”
In pure numbers, the almost 1,900 depressed subjects had fewer base pairs than their 500 non-depressed cohorts. Healthy participants’ telomeres were, on average, 5,540-base pairs long. Meanwhile, the depressed subjects’ telomeres were 5,460-base pairs long. Individuals ranged in age from 18 to 65, and corroborating prior studies into telomere-shortening, the number of base pairs reduced with each year of age, by an average of 14 pairs per year.
All hope is not lost for depression sufferers, nor those who are quickly approaching their 1,500-base pair checkpoint. Even though a person’s cells will divide roughly 50 to 70 times over the course of his or her life, at which point the cells either die or become so genetically damaged they lead to cancer, there is an enzyme called telomerase that may reverse the cellular aging process. “In young cells, telomerase keeps telomeres from wearing down too much,” wrote University of Utah science news specialist, Lee J. Siegel. “But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age.”
However, scientists believe the enzyme may be able to elongate telomeres through certain lifestyle changes. "A healthy lifestyle, such as enough physical exercise, not smoking, and a healthy diet,” Verhoeven said, “might be of even greater importance in depressed individuals than it is in the non-depressed.” What remains uncertain is whether active lifestyle changes would be contributing directly to telomere lengthening, which thereby reduces a person’s risk for depression; or whether the increased exercise, not smoking, and healthy diet bypass the telomeres — which are shortening independently — and affect depression on their own.
Part of the challenge in teasing out the underlying factors is that depression arises from a mixture of genetic, biological, environmental, and psychological factors. The disorder isn’t simply a case of the blues. It’s an illness — a chemical imbalance that requires treatment through anti-depressants targeting specific neurotransmitters, such as serotonin and norepinephrine. While scientists have come to a consensus about these chemicals, like many aspects of the brain, the specific mechanisms remain a mystery.
According to Etienne Sibellie, an associate professor of psychiatry at the University of Pittsburgh, the present study succeeds in its robust analysis. And despite a seemingly marginal decrease of 80 base pairs across both groups, Sibellie argues the “small effect” is still “real.” In terms of an active lifestyle change, he told Health Day, "it's just not known whether it has an impact on cell function.”
"If that's the case,” he said, “it has potential therapeutic importance."