Living with chronic stress can lead to many reported health effects, such as decreased cardiovascular function and reduced immune system efficiency.
Stress has even been reported to accelerate aging and the onset of age-related diseases. Recent research links both chronic and perceived stress with telomere shortening, a phenomenon with a known relationship to cellular aging.
Telomere length medical concept and telomeres located on the end caps of a chromosome resulting in aging by damaging DNA or protection resulting in living longer or longevity as a 3D illustration. Image Credit: Lightspring/Shutterstock.com
Telomeres and Psychological Stress
Telomeres protect chromosomal stability by forming protein caps at the ends of DNA. These non-coding segments are not fully replicated during replication due to difficulties with replicating the linear sequences.
This causes the telomeres to become shorter every time the cell replicates. Eventually, this leads to senescence, which is the process of biological deterioration with age. Therefore, telomeres have a profound connection to organismal aging. It was this premise, along with the known effects of chronic stress, that led researchers to hypothesize a link between telomere shortening and stress.
Indeed, researchers have since found evidence supporting this hypothesis. Both chronic and perceived stress, or self-reported measures of stress, have been linked to shorter telomeres.
Psychological stress was also linked to increased oxidative stress, which in turn has been related to increased telomere shortening. In a study on blood mononuclear cells in women, women with high stress levels were found to have telomere shortening equivalent to a decade of aging in comparison to women with lower stress levels.
Broader Causes of Telomere Shortening
Research has found that psychological stress can influence telomere length through several pathways. Apart from the aforementioned oxidative stress, research has linked other physiological effects of psychological stress to telomere length. Cortisol is one of the body’s main stress hormone with helps regulate mood, motivation, and fear.
Cortisol exposure and individual cortisol reactivity have also been found to be associated with shortened telomeres. This opens the potential for variability between individuals or groups with differing physiological stress effects. Indeed, there is some evidence that this can be true.
Stress appraisal is the process by which an individual judges stressors as threatening or challenging. The latter judgement infers that the individual feels confident in coping with a stressor, whereas the prior judgement infers they do not.
When stress appraisal and telomere length were measured in the same women, results showed that women with higher threat appraisal had shorter telomeres. This suggests that elevated threat anticipation to a stressor is another pathway by which stress can influence telomere length.
The cellular mechanism underlying how stress shortens telomere length is still not well known. Using yeast as a model organism, different environmental stressors were found to have opposite effects on telomere length. Alcohol led to lengthening of telomeres, whereas caffeine shortened them. This study did not find an effect of oxidative stress on telomere length, which has implications for the previously reported psychological studies.
While those studies had found a correlation between emotional stress and telomere length, presumably caused by oxidative stress, this study failed to establish that as the causal link. Therefore, the exact mechanism by which psychological stress is translated into telomere shortening is still unknown and needs investigating further.
While mechanisms regulating telomere shortening are still elusive, certain studies have started addressing this question. Regardless of whether the stressor led to shortening or elongation of the telomeres, the telomere length machinery genes which were differentially expressed because of the stressor were clustered near each other. This suggests that these telomere length machinery genes are involved in the phenomenon of telomere alteration in response to stress.
Within these clustered genes, however, there is some disagreement on what causes the differed telomeric length. For example, the research found the telomere length machinery mutant, rif1Δ, to respond normally to elevated temperature stress but responded less to caffeine and alcohol stress.. The Rif1 protein is necessary for both shortening and elongation but seems to be implicated in a sensing or regulatory role rather than a catalytic one when responding to stress. Therefore, it may have a critical role in telomeric response to psychological stress as well as environmental stress.
Psychological stress can impact telomere length through more indirect routes, as well. Herpes virus cytomegalovirus (CMV) and Epstein-Barr virus (EBV) can cause boosted replication of memory T-cells, which can exhaust the virus-specific T-cells. Therefore, chronic exposure to these viral antigens can cause increased replication, which leads to shortened telomeres in T-cells.