In each of the human body’s cells there are 23 chromosomes, which are twisted, double-strands of DNA molecules. Chromosomes are vital as they provide our singular genetic map to every cell within our body. Lucky for us, on the ends of each of our chromosome strands sits a protective cap called a telomere. This cap protects our genetic data and literally keeps our chromosome DNA strands from fraying, becoming dysfunctional and even dying.
You can think of a telomere as the plastic tips on both ends of a pair of shoelaces. Without the reinforced tip the shoelaces will fray and not perform well. Without telomeres the chromosome ends will fray and even stick to each other, destroying genetic information (or causing corrupted genetic information to be passed along).
Every time our cells replicate themselves – which is constantly happening in many cells throughout the body in order for us to live – our telomeres get just a little bit shorter. Eventually the telomeres get too short to function, causing the cell to age and then stop functioning altogether.
So our telomeres shorten naturally as we age chronologically.
Scientists have also found that along with our chronological age, there are other factors that contribute to shortened telomeres, such as stress, a poor diet/obesity, lack of exercise and smoking.
Do shorter telomeres result in aging? Or does aging result in shorter telomeres?
Scientists have done a lot of research on telomeres. The question they have looked at is whether shorter telomeres actually cause aging, or are shorter telomeres just another marker for aging, like grey hair?
Scientists don’t have the answer to this question as yet, but the two (shorter telomeres and aging) are definitely linked. Laboratory and clinical research have proven linkages across many studies.
As one simple example of how aging and telomere length are connected, in white blood cells, normal telomere length ranges from 8,000 based pairs in newborns, to 3,000 based pairs in adults, and as low as 1,500 in the elderly.
A chromosome has some 150 million base pairs to start with; with cells normally dividing about 50 to 70 times. In all cells that normally divide, telomeres shorten with these divisions. Note that some cells in the body, such as heart muscle, do not divide and do not show decreases in telomere length with age.
In younger cells, an enzyme called telomerase keeps telomeres from shortening too much, but as cells divide there is less telomerase with each division; there is also a decrease in telomere length.
The importance of telomerase in species survival, health and cancer
Scientists have looked at the role of the enzyme telomerase in both healthy and cancerous cells.
In reproductive cells (sperm and egg cells), there is a high level of telomerase, which helps maintain telomere length. This ensures healthy cells are passed from one generation to the next. Scientists believe that this supports species survival.
They have also found that some cells have more telomerase than others. For example, stem cells (which are viewed as regenerative in nature) usually have high levels of telomerase. This likely helps prevent the shortening of the telomeres in stem cells, allowing stem cells to live longer.
In cells that become cancerous, scientists have found that the cell divides much more often and its telomeres become very short more quickly. Given this signals that the cell may soon die, the body tries to thwart this by producing more of the telomerase enzyme. The telomerase enzyme prevents the telomeres from getting any shorter and saves the cancerous cell from dying. It actually makes the cell become “immortal”. Most malignant tumors – including colorectal cancer, breast cancer, prostate cancer and ovarian cancer – exhibit such increased telomerase activity. And the more advanced the cancer is, the more telomerase is found.
So if increasing telomerase in a cancerous cell promotes its survival and so-called “immortality”, could decreasing the enzyme actually kill off cancerous cells?
Scientists have been studying whether reducing telomerase could be a key to killing off cancer cells. They have already shown that blocking the production of telomerase can in fact cause some cancer cells (breast and prostate cancer) to die in laboratory experiments. But blocking telomerase has many negative side effects, such as impacting a lot of good things going on in the body. A few of these include the production of immune system and blood cells, wound healing and fertility.
Can telomerase be the fountain of youth?
If the enzyme telomerase can make cancer cells survive and become immortal, scientists have wondered, could it prevent normal cells from aging by keeping telomere length intact? Studies looking at lifespan and telomere length have shown that people with longer telomeres live a longer life.
But most scientists agree that telomere length is just one piece of the aging puzzle. Most believe that oxidative stress has a much larger impact. Oxidative stress is damage to our DNA, lipids and proteins caused by oxidants; oxidants being things like inflammation, poor diet, infections, smoking, alcohol, toxins in the environment, etc.
On top of these other impacts there is the question of promoting cancer in otherwise healthy cells. Would increasing telomerase enzyme promote cancer in otherwise healthy cells? Scientists aren’t sure. Initial laboratory studies have not shown this to be true.
More research is needed.
Sounds like scientists aren’t sure of a lot. What do we really know?
Scientists know there is a correlation between telomere length and chronological age. The older you get the shorter your telomeres.
There is no proven cause and effect, however, just a linkage. Which influences the other is not known. And to what extent the enzyme telomerase plays a direct role on aging is also unclear. People with genetic mutations affecting the enzyme telomerase have much shorter telomeres and suffer from accelerated aging issue, so is the enzyme itself causing aging?
Scientists do agree that “chronological age” does not equal “biological age”. Some 60 year olds are vibrant and others are not. The factors involved in this difference certainly include lifestyle decisions – which affect oxidative stress – such as diet, exercise, stress, vices (smoking, alcohol, drug use, etc.), and toxin exposure in one’s foods and environment.
And the health of our cells also plays a role. Inheritable aspects relating to our telomere length and telomerase levels (some speculate the percentage of inherited attributes to be quite high) likely play a role, as does the ongoing shortening over time related to age.
Why does it matter?
Scientists believe that studying telomeres is key to both understanding aging as well as treating conditions of aging such as heart disease and diabetes. Someday, perhaps targeted efforts using regenerative stem cells – high in telomerase – could extend the life of telomeres related to specific diseases, for example. There is already evidence linking shortened telomeres to Alzheimer’s disease, high blood pressure, type 2 diabetes and hardening of the arteries.
Additionally, better understanding how lifestyle changes affects telomerase activity and telomere length could provide improved therapies in addressing many health complaints and diseases. Studies have already shown this to be true. For example, in a 2013 study by UCSF it was found that men with low-risk prostate cancer who made comprehensive lifestyle changes kept their telomere length higher. And there are many other examples.
Bottom line is that telomeres keep us alive by providing a “protective zone” of sorts for our DNA. It will be interesting to see how all of the research plays out relating to how we can leverage telomere health to heal and perhaps extend our lives.