Stress, Cellular Ageing and Mindful Meditation (SQ-11)

Heavy workloads, meeting tight deadlines, care giving, financial worries.

Stress has invaded our daily lives in many forms. We can withstand occasional bouts of extreme stress, which can actually be a good thing by motivating us to take meaningful action. But what happens when we are frequently or continually exposed to such environmental stressors? It takes a toll on our health. Stress plunges the body towards poor health and premature aging. Scientists warn us that it is important to find ways to manage and reduce chronic stress in our lives or else risk the onset of many age-related diseases such as dementia, cardiovascular diseases, diabetes, arthritis, depression and even cancer.

In a nutshell, stress is bad news! If you are experiencing ongoing stress, it is not only damaging your health but literally pushing you towards premature aging. Does it mean we can actually control our biological clock in some ways by managing our stress? We are not actually seeking to reverse the clock but delaying the premature aging brought on by stress. So, is it possible?

Emerging studies in this field show that telomeres - protective caps at the end of our chromosomes - may provide a pathway to explore this question. More specifically, the length of telomeres is considered as a biomarker for aging and possibly a predictor of future health. And studies show that stress is known to shorten telomere length. Let’s find out the fascinating relationship between cognitive stress, telomeres and rate of cellular aging. And how mindful mediation fits this landscape.

Telomeres: Our biological clock?

Telomeres are the protective caps of proteins at the fragile end of each strand of DNA. Telomeres prevent the chromosomes ends from sticking to each other, an action that would corrupt the genetic information. Scientists liken them to aglets, the plastic tips at the end of shoelaces that protect the tips from fraying. But telomeres serve another very important function during cell division.

Cells in our bodies divide for many reasons. They divide so that we can grow or to replace old, dead or damaged cells. In fact our body is constantly substituting old, damaged cells with new ones at the rate of millions per second. While it sounds like a lot of work, what goes on backstage is even more meticulous, yet so fascinating.

1. The nucleus of all living cells have DNA molecules, tightly packed into thread like structures called chromosomes. Humans have 23 pairs of chromosomes.
   
   
2. DNA contains thousands of genes that carry our genetic information (instructions).
   
   
3. A DNA strand is made of 4 nucleotide bases: adenine (A), thymine (T), guanine (G) and cytosine (C). The bases on one strand of DNA pairs with bases on the other strand to give rise to a double helix structure. What is interesting here is that A always pairs with T while G always pairs up with C. The sequence in which these base pairs are arranged is a kind of blueprint or set of instructions to make thousands of proteins responsible for our traits, such as blond hair, brown eyes or height.
   
   
4. Before a cell divides, it duplicates its chromosomes so that the resulting new cells have identical genetic information. To achieve this, the two DNA strands must unzip and separate.
   
   
5. An enzyme, DNA polymerase, then helps to duplicate DNA strands but can’t continue the replication all along the length of the chromosome.

A complex process that ensues results in cell division but each time a cell divides, the chromosomes are shortened by about 25-200 bases. This is where telomeres play a protective role. The ends of chromosomes are capped by telomeres so the only section that gets snapped is from the telomere length – leaving the main DNA strand intact. Telomeres are basically stretches of DNA that have the same sequence of bases repeated over and over. If not for telomeres, some part of DNA would be lost every time a cell divides – resulting in loss of important genetic information and eventually the entire genes. So, telomeres get slightly shorter with every cell division until a stage comes when telomeres becomes too short. At this point in cell division, the chromosomes reach a critical stage and can’t replicate any more. This triggers the cell to undergo senescence (aging) or apoptosis (programmed cell death).

Our story is about to get even more exciting with the entry of telomerase, an enzyme that protects and rebuilds telomeres by adding telomeric DNA or repeat sequences of bases to shortened telomeres – thus maintaining their length. The longer the telomere, the more times a cell is able to divide and renew itself. “Telomerase is a ribonucleoprotein reverse transcriptase cellular enzyme that counteracts TL shortening and adds telomeric DNA to shortened telomeres. Telomerase thus forestalls shortened telomeres from signaling the cell to cease dividing or to die. Telomerase promotes cell longevity even in the face of critically shortened telomeres.” [1]

In 2009, three scientists - Elizabeth Blackburn, Carol Greider and Jack Szostak - received the ‘Nobel Prize in Physiology or Medicine’ for their remarkable work in this field. They showed that chromosomes are protected against degradation by telomeres and the enzyme telomerase [2]. As we age, the amount of this protective enzyme declines, restricting the ability of cells to replenish and maintain telomeres. Low telomerase activity and shortening of telomeres makes the cells susceptible to fusions, aging and death.

Scientists consider the length of telomeres as one important metric in aging and possibly a predictor of future health. Shorter telomeres have been associated with the onset of many chronic age-related conditions such as cardiovascular disease, type 2 diabetes, osteoarthritis, dementia and high blood pressure.

What else accelerates telomere shortening?

Besides natural cellular aging, there are many lifestyle related factors that are known to trigger shortening of telomeres, such as poor sleeping patterns, poor diet, smoking, alcohol and a sedentary lifestyle. In 2004, Elizabeth Blackburn and team showed that chronic psychological stress, commonly associated with premature aging, poor immune functions and risk of developing many age-related diseases, may lead to shortening of telomeres [3].

But here is some good news. We have some very promising and prominent studies that show that mindful meditation can actually help us manage stress and may have positive effects on telomere length and the activity of telomerase.

Mindful Meditation and Stress: How does it all fit together?

So, what exactly is mindful meditation? Derived from a century old Buddhist practice, it is a technique that involves slow, regular breathing while focusing on the present moment in a non- judgemental manner. In other words, mindful meditation or mindfulness makes one aware of the present. The practice allows the mind to voluntarily shift its assessment of a stressful situation from a threat that triggers stress, anxiety and unproductive worry to acceptance. It also increases positive emotions and decreases rumination – which is the tendency of the mind to keep wandering back to negative thoughts. According to Buddhist traditions, meditation decreases psychological distress and promotes well-being [4]. The question is, can mindfulness slow down the rate at which a cell ages? Can it actually influence telomere length?

A 2009 study shows that mindfulness can reduce stress arousal and it may slow the rate of cellular aging by increasing the levels of telomerase, a protective enzyme that protects telomeres and even help rebuild them [5]. Another 2014 study showed that mindfulness meditation leads to increased telomerase activity in peripheral blood mononuclear cells [6].

A 2016 study by Spanish researchers showed that expert Zen meditators had longer telomeres than a group of people who had never meditated but otherwise were similar in age and lifestyle [7]. On crunching the data, the analysis suggested that age, absence of experiential avoidance and high self-compassion were top factors that were directly responsible for the link between meditation and long telomeres. Experiential avoidance is our natural instinct to cope with painful memories, negative emotions and sensations by simply supressing them and not letting them come to fore. While this tendency may be temporarily helpful, it spells trouble over the long term. Mindfulness, on the other hand, takes one to a path of accepting the present in a non-judgmental way.

Besides promoting telomere length and increasing telomerase activity, mindful meditation is also known to change our brain structure allowing for positive emotions and improved memory and concentration. A 2011 study published in ‘Psychiatry Research: Neuroimaging’ suggests that mindful meditation can bring changes in “gray matter concentration in brain regions involved in learning and memory processes, emotion regulation, self-referential processing, and perspective taking.” [8]

Stress also contributes to chronic inflammatory conditions. A 2016 study showed that long-term meditation results in small cortisol activity and reduced inflammatory and stress response to stressors, and concluded that “long-term practice of meditation may reduce stress reactivity and could be of therapeutic benefit in chronic inflammatory conditions characterized by neurogenic inflammation.” [9]

A very recent 2016 study suggests that mindfulness may be an effective intervention to treat post-traumatic stress disorder (PTSD) [10]. It showed that mindfulness training stimulated positive changes in neural networks in participants who were combat veterans with PTSD deployed to Afghanistan and/or Iraq. These changes in brain connectivity allowed the participants to make a shift from negative emotions and repetitive loop-like thinking and rumination.

As aptly summarized in 2009 study titled “Can meditation slow the rate of cellular aging? cognitive stress, mindfulness, and telomeres”, “Stress cognitions are important for survival, but if they are based on distorted perceptions, they may promote excessive stress arousal, creating a harmful milieu for cellular longevity…….H.H. the Dalai Lama explained that emotions based on reason and analysis, tend to drive meaningful behaviour. In contrast, emotions based on ‘false projections’ or fear-based beliefs are harmful to longevity.”

Meditation sounds a great way to cope with life stress and delay premature aging and improve the quality of life. Isn’t it surprising what a few calm, relaxing moments can do to positively shape our health?

References:

1. Elissa Epel, Jennifer Daubenmier, Judith T. Moskowitz, Susan Folkman and Elizabeth Blackburn. Can meditation slow rate of cellular aging? Cognitive stress, mindfulness, and telomeres. Ann N Y Acad Sci. 2009 Aug; 1172: 34–53.
2. The Nobel Prize in Physiology or Medicine 2009. NobelPrize.org
3. Elissa S. Epel, Elizabeth H. Blackburn, Jue Lin, Firdaus S. Dhabhar, Nancy E. Adler, Jason D. Morrow and Richard M. Cawthon. Accelerated telomere shortening in response to life stress. PNAS 2009.
4. Dalai Lama and Cutler, 2009.
5. Epel et al. Can meditation slow rate of cellular aging? Cognitive stress, mindfulness, and telomeres. Ann N Y Acad Sci. 2009 Aug; 1172: 34–53.
6. Schutte NS, Malouff JM. A meta-analytic review of the effects of mindfulness meditation on telomerase activity. Psychoneuroendocrinology. 2014 Apr;42:45-8.
7. Alda et al. Zen meditation, Length of Telomeres, and the Role of Experiential Avoidance and Compassion. Mindfulness. February 2016
8. Hölze et al. Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry Research: Neuroimaging. 2011.
9. Rosenkranz et al. Reduced stress and inflammatory responsiveness in experienced meditators compared to a matched healthy control group. Psychoneuroendocrinology. 2016
10. King et al. ALTERED DEFAULT MODE NETWORK (DMN) RESTING STATE FUNCTIONAL CONNECTIVITY FOLLOWING A MINDFULNESS-BASED EXPOSURE THERAPY FOR POSTTRAUMATIC STRESS DISORDER (PTSD) IN COMBAT VETERANS OF AFGHANISTAN AND IRAQ. Depression and Anxiety. 2016.

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