Getting Long in the Telomeres

Editor’s note: Pending an FDA decision, 23andMe no longer offers new customers access to health reports referred to in this post. Customers who purchased prior to November 22, 2013 will still be able to see their health reports, but those who purchased after that time will not. Those customers will have access to ancestry information as well as access to their uninterpreted raw data.

Robin Smith, Health Content Scientist

Barring injury, disease or capture, some scientists believe that a lobster could live virtually forever. They are amongst a select group of animals, including tortoises, clams and jellyfish, that are “negligibly senescent.”

Chromosomes tipped by telomeres.

Chromosomes tipped by telomeres (in white).

They don’t age much. So why aren’t we so lucky?

Unlike lobsters, our cells have a limited ability to replicate and renew themselves over the course of our lives. One cause of this limitation lies in our telomeres: DNA segments at the ends of our chromosomes that get shorter with each replication. When a cell’s telomeres get too short, it can no longer replicate and eventually dies. A few cells — namely adult stem cells as well as sperm and egg cells — are not limited by this process, though. These cells have an enzyme named telomerase that can rebuild telomeres when they get too short. This process is hijacked by cancer cells, which become effectively immortal by turning on telomerase.

There are several indications that telomere length is a good predictor of longevity. In newborns, telomere length varies from about 8,000-13,000 “base pairs” (DNA letters) in length, and declines by about 20-40 base pairs each year. Telomeres are also longer in women than men, mirroring the difference in lifespan between the sexes. In elderly twins, the twin with shorter telomeres is roughly three times more likely to die first.

The variability in telomere length between people of the same age is not random, and has a genetic component that has interested scientists for decades. In a recent study in the journal Nature Genetics, scientists identified multiple markers that are associated with either shorter or longer telomeres. The strongest of these () resides near a gene named TERC. Each copy of a “T” at this position is associated with an average 117 base pair decrease in telomere length, equivalent to having the “biological age” of a person about four years older.

A person’s genetic makeup is not the only determinant of telomere length: environmental factors such as smoking and obesity bring about premature telomere shortening. Telomere length is also highly influenced by the age of the father at conception. Because sperm cells are one of only a few types of cells that maintain or even increase their telomere length over time, the trend is for older fathers to have children with longer telomeres. This effect can even carry over a second generation to grandchildren. It’s interesting to speculate that the trends in some societies towards delaying parenthood may have the unexpected benefit of boosting life expectancy. Any such benefit, however, would have to be weighed against known risks of being an older dad.






  • http://wellnow.be/ Dave S.

    Fascinating blog post, made all the more fascinating because my 23andMe results now include info on my telomere length.

    But I have a question. You say, “A few cells — namely adult stem cells as well as sperm and egg cells — are not limited by this process, though. These cells have an enzyme named telomerase that can rebuild telomeres when they get too short.”

    My understanding is that all cells have telomerase, but that they run out of it or stop producing it over time. So what’s happening with adult stem cells and sperm and egg cells? Are they in some sort of harmonious balance of telomerase production: more than normal cells but less than cancer cells?

    • http://23andMe.com Robin Smith

      Hi Dave,

      As the author of the blog post, I’d be happy to answer your question.

      The short answer is that while all cells in the adult human body have some detectable amount of the telomerase, really only a handful of normal (non-cancerous) cells have enough telomerase to prevent the normal rundown of telomere length over time.

      But you bring up a very good question. What’s special about the cell types that can express telomerase but do not become cancerous? It’s important to keep in mind that while adult stem cells can generate more copies of themselves than normal cells, they cannot do so forever. These cells generally have a need to replicate a lot (e.g. in the immune system and skin), and our physiology has accommodated that process during millions of years of evolution. Their telomeres do shorten over time, just at a much slower rate than other cells in your body. This is accomplished by tightly controlled bursts of telomerase that the cells produce every time they make a copy of themselves (see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370415/). The worst cancer cells, on the other hand, are telomerase factories, making them actually immortal. If you haven’t heard of HeLa cells, I encourage you to look them up (http://en.wikipedia.org/wiki/HeLa). So in effect, you are correct that the telomerase levels in adult stem cells are in a balance somewhere between normal cells and cancerous cells.

      Telomeres are long in spermatozoa due to the continuous expression of telomerase in the cells that produce them in the testis (see http://www.ncbi.nlm.nih.gov/pubmed/8934879). The specifics of how this leads to a lengthening of telomeres over time is an interesting topic that is the subject of ongoing research. After fertilization of an egg, embryonic stem cells in the blastocyst express telomerase at high levels. As the embryo develops, these cells eventually lose their “stemness” and specialize and become of an organ. In doing so, their telomerase levels taper off, causing their telomeres to gradually shorten each time the cells copy themselves.

      Robin

  • darkeyes

    Hi. I don’t have the Ts for the TERC SNP, am mixed on the other SNPs for telomere length, and look too young for my age, being mistaken by some people for being just out of school. However, I know I am aging, and am accepting of this. I intend to make the most of my life until I go just like my ancestors. There is a fine line between elongating telomeres indefinitely and creating cancer, and we have not come up with an answer as of yet. Let’s live our lives to the max and be grateful for what we have.

  • Nalliah Thayabharan

    DNA structures that cap the ends of chromosomes known as telomere plays an important role in cell division, and in the aging process by preventing the DNA from unraveling and fusion with neighboring chromosomes. During cell division, enzymes that duplicate DNA cannot continue their duplication all the way to the end of chromosomes. If cells divided without telomeres, they would lose the ends of their chromosomes, and the necessary information they contain. The telomeres are disposable buffers blocking the ends of the chromosomes, are consumed during cell division, and an enzyme known as “telomerase” actively restores it. In life, there’s an ongoing battle between telomeric loss and telomerase-based restoration. If your telomeres degrade beyond a critical point, cell division is no longer possible.

    Average telomere length is individually variable, and is inherited. Not surprisingly, given a base rate of telomerase activity, the longer an individual’s telomeres, the more degradation can be hypothetically tolerated, and the greater their lifespan.

    If dad has long telomeres and mom has short ones, when their DNA combines in that egg that becomes you, are yours going to have long telomeres like dad since telomeric length will be correlated with your father’s, and not with your mother’s. For both females and males — look to your father for a prediction of your own longevity.The telomeres in a man’s sperm get longer the older he gets, and this means his offspring will have longer telomeres but it carries risk of genetic mutation.

    People with shorter immune cell telomeres die earlier than people with longer immune cell telomeres. Also health behaviors such as exercising, eating a healthy diet and reducing psychological stress may influence how quickly our telomeres shorten or lengthen.

    HOWEVER, you should know that telomere length does NOT predict the probability of the onset or progression of senility. This may be because the brain is less dependent on cell division across a lifetime than are other body organs. It strongly indicates that cellular senescence attributed to a long history of cell division is NOT a primary source of origin of Alzheimer’s Disease. It’s always cheering to know that you may be genetically set up for a long life. At the same time, you had better get to work on your brain fitness strategies, to insure that those extra years are spent fruitfully, because living long provides very little assurance that you’ll be living well!.

  • RM Cawthon

    What method is 23andMe using to measure telomere length?

    • ScottH

      RM, 23andMe doesn’t measure telomere length. What we do is report out an association between shorter telomeres and a certain genotype. The report on biological aging looks at a specific SNP, rs10936599 is located near a gene called TERC, which encodes encodes part of the telomerase enzyme. This enzyme is what keeps telomeres from getting shorter.

  • Scientist

    Why doesnt 23andme.com analyze the actual telomere lenght (but only a telomerase-associated SNP)?

  • Luis Chavez

    The article says that we are born with 8000 to 13000 base pairs and lose about 20 to 40 base pairs per year. 8000 base pairs/40 base pairs per year = 200 years…Why don’t we live to be 200 years? Do we lose more base pairs in the later years? Please let us know. Thanks!

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