Telomeres are an Integral Part of Aging and Disease
We are always looking for ways in which we can thwart the progression of aging. With each cell generation, the telomere gets shorter and shorter until it can no longer maintain the integrity of the chromosome. It is then that apoptosis occurs. There are many supplement and exercise recommendations on the market at the present time that claim to lengthen and/or strengthen the telomeres. The only way in which to know if that is indeed happening is to do a molecular test that has the capability to accurately measure telomere length. IndigoBridge Laboratories offers a state-of-the-art telomere test that can provide those answers.
Telomeres were initially discovered at UC Berkeley by Elizabeth Blackburn in the 1970s (4). This was followed by the discovery of the existence of a compensatory mechanism for telomere shortening which was first found by Soviet biologist Alexey Olovnikov in 1973 (5,6). Olovnikov also suggested the telomere hypothesis of aging and the telomere's connections to cancer (6). Then in 1984, Blackburn’s group discovered the enzyme telomerase (telomere terminal transferase) (4). This enzyme was, according to the Blackburn studies, able to add DNA back onto telomeres (4). It was not until1997 that the catalytic protein component, shelterin, was isolated, first in yeast (7) and shortly thereafter in humans (7,8). In 2009, Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak were jointly awarded the 100th Nobel Prize in Physiology or Medicine for their discovery of ‘how chromosomes are protected by telomeres and the enzyme telomerase’ (3). Telomeres are the regions at the ends of chromosomes, consisting of many repeats of a short nucleotide sequence coupled with an associated protein complex known as shelterin (or telosome). They are often likened to the plastic cap on the ends of shoelaces that prevent the shoelace from unraveling, as they play a similar role to protect the chromosome ends. In some ways, telomeres are the weak link in DNA. They are readily damaged and must be repaired, yet they lack the repair efficiency of other DNA. This results in an accumulation of partially damaged and poorly functioning telomeres of lower quality, regardless of length (34). Telomeres are shortened every time our cells replicate. It is well documented that telomeres progressively shorten with increased cellular age both in vitro and in vivo (27), and studies have demonstrated that telomere length is inversely correlated with lifespan (28). In 1961, Leonard Hayflick and his colleague Paul Moorehead discovered that cultured normal human cells have a limited capacity to divide, and that cryogenically preserved cells remembered the number of times that they had divided at the time they were frozen (11). In what is now known as the “Hayflick Limit,” after a certain number of divisions, cells engage a new pathway termed replicative senescence (9,10). This withdrawal from the cell cycle is known to be triggered by shortened telomeres (11,12). Cancer cells have evolved the ability to overcome senescence (13) by using mechanisms capable of maintaining telomere lengths (such as expressing telomerase), which is one of the characteristics that enables cancer cells to divide indefinitely (13-16). Telomerase activity is absent in most normal tissues or is highly regulated in normal transit-amplifying stem-like cells (27). However, a critical step in oncogenesis involves the up-regulation or reactivation of telomerase in order to bypass the pathway to replicative senescence, and approximately 85–90% of all tumor biopsies are telomerase positive (32). This ability, along with the unique universal presence of ENOX2 proteins (17-24), is a biomarker for almost all advanced human cancers. Multiple mutations must occur for a cell to transform and become malignant; telomere shortening may also be a common underlying cause of chromosomal rearrangements in cancer (25,26). So, in combination with a series of oncogenic changes, some cells with short telomeres escape senescence and become immortal, usually by activating or upregulating telomerase (27). Prevention of aging, by definition, translates to longer lifespan! The early work that demonstrated the causal relationship between telomere shortening and cellular aging was published in 1998 by Bodnar et al. (35). In recent years there have been many studies that have shown that these nucleotide sequences can also be shortened by an unhealthy lifestyle: poor diet, lack of exercise and sleep, smoking, obesity, and stress(29). But research also suggests that if we intervene with diet, exercise, and targeted supplementation, we can lengthen telomeres and thereby prevent aging. Elizabeth Fernandez wrote an article entitled “Lifestyle Changes May Lengthen Telomeres, A Measure of Cell Aging: Diet, Meditation, Exercise Can Improve Key Elements of Immune Cell Aging, UCSF Scientists Report.” It referred to a small pilot study that showed for the first time that changes in diet, exercise, stress management and social support may result in longer telomeres. This 2013 study was the first controlled trial to show that any lifestyle or dietary intervention might lengthen telomeres over time. Since then, many other studies have demonstrated these findings, including studies out of such prestigious institutions as Brigham Young University, journals such as the American Heart Association publication Circulation, and the European Heart Journal. These studies demonstrate that lifestyle interventions such as exercise, meditation, yoga, nose breathing to increase nitric oxide, diet, (including a focus on healthy methylation status), taking supplements such as SAMe, B12, folic acid, magnesium, and zinc can impact telomere length as well as telomere quality, and that interventions are capable of epigenetically marking the telomeres for proper function and, in essence, turning back the biological clock. This can be done by improving the activity of the telomerase enzyme which can add length back to telomeres (36-42). More and more research lends credence to the thought that expression of telomerase in normal cells may extend healthy lifespan, especially for patients with inherited telomere spectrum disorders (27). And with the obvious anti-cancer nutrients that have come to light, such as the green tea catechin EGCg, it makes sense to measure telomere length and do what is necessary to lengthen and strengthen them, while concomitantly taking chemoprotective agents such as green tea concentrates (24,31,). One study showed that even short-term (∼2 weeks) expression of telomerase in normal cells is sufficient to double the proliferative lifespan of cells (27). And so, it has been known for many years now that nutrition can have a significant impact on the length of telomeres. In the book The Telomere Effect (2017) by Elissa Epel and Elizabeth Blackburn, the researchers recommend a plant-based approach that includes fresh vegetables, fruit, whole grains, nuts and legumes. In addition, other nutrient-rich foods that are high in antioxidants such as seaweed and green tea have also been linked with longer telomeres and increased lifespan.