According to The American Institute Of Stress,
“All the cells in our body contain tiny clocks called telomeres that can determine how long they will live. Telomeres are little caps at the end of chromosomes that prevent loss or injury to genetic information during cell division. Each time a cell divides, part of the telomere is lost and it becomes shorter. When a telomere eventually disappears because of repeated cell divisions, chromosomal damage prevents the cell from accurately reproducing itself. This shortening and eventual erosion of telomeres is prevented or reduced by telomerase, an enzyme in cells that preserves their length. Many believe that telomere destruction and reconstruction is related to the balance between aging and cancer and explains why cancer is more common in the elderly.”
Replicative senescence is the stage where cells lose the ability to divide further, and experts believe that this process is what wears cells out and contributes to shorter life spans and premature aging. Cells with long telomeres are healthy and live longer, but shortened telomeres have been linked to serious medical complications and disease, including type 2 diabetes, osteoporosis, compromised immunity, and coronary heart disease.
According to the American Diabetes Association, “aging is a major risk factor for a number of complex diseases including cancers, cardiovascular disease, and type 2 diabetes, yet the biological processes linking aging and disease risk are poorly understood. A potential mediator of age-related increases in disease risk may lie in repetitive sequences of DNA known as telomeres.”
While telomeres naturally shorten in older age, (Determination of telomere size in humans: a twin study of three age groups; Slagboom PE, et al) the rate of the shortening process does vary from one person to the next (Rise in insulin resistance is associated with escalated telomere attrition; Gardner JP, et al).
According to the American Psychological Association, “A number of studies have linked stress with shorter telomeres, a chromosome component that’s been associated with cellular aging and risk for heart disease, diabetes, and cancer.”
Researchers from UCLA have not only confirmed prior findings that subjects living with chronic stress have shorter telomeres, but they have also discovered the mechanism that explains just how this occurs.
The shortening of telomeres is prevented or lowered by a process known as telomerase that keeps cells young by preserving their length and maintaining their ability to effectively divide and reproduce.
The UCLA study found that secretion of the stress hormone cortisol suppresses telomerase activation in immune system cells, which leaves them unprotected during cell division and so over time they become shorter leading to premature cell aging and distorted cell replicas that increases risks for cancer and other chronic diseases.
A 2012 study, published in the journal PLoS ONE, discovered that subjects with the most job stress had the shortest telomeres, and those short telomeres caused cells to die.
Elizabeth Blackburn, Nobel Prize winner in Physiology or Medicine 2009 and author of The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer (with Elissa Epel) who is currently the President of the Salk Institute for Biological Studies told The Guardian, “Nobody had any idea that meditation and the like, which people can use to reduce stress and increase wellbeing, would be having their salutary and well-documented useful effects in part through telomeres. The book is also recognizing how much control we can have. Small tweaks in how you approach stress, for example, can lead to long-term habits that make a difference.”
Anticipation Of Stress May Accelerate Cellular Aging
Another study (Elissa Epel, et al) published in Brain, Behavior, and Immunity found that 50 female subjects who were most threatened by anticipated stress related to public speaking, and solving math problems had shorter telomeres.
More interesting is the fact that half of the study subjects were caretakers of people with dementia and so had higher levels of stress anticipation than subjects who were not, which suggests that those with chronic stress levels are more susceptible to cellular aging from higher levels of anticipated stress in everyday life.