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Do stress and telomerase go together?

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It seems that humans have, throughout their life history, suffered from a lot of stress. First there were lions and tigers and bears, then there were other humans with pointy metal objects, and now there are deadlines and traffic jams and bankruptcy. Stress, even the kind of stress many of us deal with nowadays, can be rough on the body. It can produce depression, anxiety, increased sensitivity to illness, and it even can shorten your life expectancy. None of these are good, and many of them are related to cell aging and death.

But our bodies do their best to work around these negative effects. And one new way? Extra telomerase. But there is a way to combat cellular aging, and that’s via something called telomerase. But is it meaningful? That’s a good question.

Beery et al. “Chronic stress elevates telomerase activity in rats” Biology letters, 2013.
(Side note: Nobel Prize winner Elizabeth Blackburn is on this paper! No surprise there, telomeres are right up her alley!)

To know about telomerase you have to know about telomeres. When cells replicate, the DNA within them replicates first (during the S phase). The DNA then forms up into chromatids, which form into X-shaped pairs and get pulled apart during replication, 1/2 of the DNA to each new cell. But during that time, when the DNA is replicating and in chromatids, there are telomeres.

Telomeres are random sequences of DNA at the end of your REAL DNA. They form an incredibly protective cap, and so though they may “say” nonsense, they mean a lot. The enzymes that perform DNA replication can’t go to the very ends of the DNA, they have to stop before they reach the end. If your DNA just ended where it needed to end, with nothing else there, each time replication occurred, you would lose some of your DNA. Some of your important, coding DNA. If you lost a little bit of your genome every time a cell replicated…well none of us would be here at all. So you have telomeres, nonsense DNA strands which get slightly shorter with every replication of the DNA.

(You can see them there on the ends. Source)

Of course, you don’t want to lose your telomeres either, as then you’d start losing regular DNA. And in fact, telomeres getting shorter is a sign of aging. So there are actually enzymes that help to maintain and lengthen your telomeres, called telomerases. Telomerases can save us a lot of grief, lengthening our telomeres and protecting our cells from senescence (when cells get too old to divide). Deficiencies in telomerase can be associated with many problems including premature aging and severe immune deficiency. So high levels of telomerase are protective, promoting long life for a cell.

And this could be meaningful for stress. We know that stress can cause cell death of various types, could telomerase help? And this led the authors of this study to ask about stress. We know that stress increases signs of cell aging and death. And we know that telomerase often increases, to lengthen telomeres and presumably prevent cell aging and death. So what happens to telomerase when you are stressed?

To examine this, the authors of this study took rats and exposed them to chronic stress (what I like to call the rat equivalent of academia). The rats never know what they’re getting on any given day. Sometimes they have to swim, sometimes their cage is tilted. Sometimes they get rock music all night, and sometimes they have to smell the smell of a predator (in this case, fox odor, and I pity ANYONE who has to work with this stuff. It never comes out of anything. Ever). This type of unpredictable stress is hard on rats (not to mention hard on the humans who have to do all the changing, often at very odd hours). The stressed rats didn’t gain as much weight as their relaxed controls, and showed high levels of anxiety in the elevated plus maze, open field, and light dark box.

You can see the measures of open field, elevated plus maze, and light dark box above (left to right). These are all anxiety measures in rats that take advantage of a rat’s natural aversion to bright light and open spaces. The more anxious a rat is, the less time he will spend in the middle of an open field, on the open arms of an elevated maze, or in the light part of a box. You can see that the stressed rats were much more anxious than their related counterparts.

And these behavioral effects were correlated with increased telomerase activity. The more stressed behavior the rats showed, the more telomerase activity they had.

Now, this doesn’t mean that stress directly causes telomerase activity or that telomerase activity causes stress. But it could mean that increased telomerase activity is one way for cells to deal with the difficulties of stress, increasing telomerase activity to protect the DNA from excessive destruction, and protect cells from senescence. It merely means that when they stressed animals, there was increased telomerase activity. As pointed out in the comments, a lot of things increase telomerase activity, and since stress IS still associated with cell aging signs and cell death, whether or not those increases in telomerase activity are meaningful is unclear. It would be interesting to see if increasing telomerase activity prior to stress could protect animals from the effects of stress (like, say, the effects of stress on neurogenesis, where stress causes major decreases). That would be the way to show that telomerase plays a meaningful role in the effects of stress. But for now, it’s another role for telomeres, and for telomerase. Protecting your telomeres to save you from stress. So, while the two things, stress and increased telomerase, go together, whether they MEAN anything together is less certain.

Beery, A., Lin, J., Biddle, J., Francis, D., Blackburn, E., & Epel, E. (2012). Chronic stress elevates telomerase activity in rats Biology Letters, 8 (6), 1063-1066 DOI: 10.1098/rsbl.2012.0747

EDIT (3/26/13): As people have pointed out in the comments, there is no established LINK between stress and telomerase activitiy. The two are merely shown here to co-occur, and to suggest that the telomerase activity here might be meaningful is too much speculation. I have changed the title and edited parts of the post to reflect this. Corrections throughout the post are in italics.

Scicurious About the Author: Scicurious is a PhD in Physiology, and is currently a postdoc in biomedical research. She loves the brain. And so should you. Follow on Twitter @Scicurious.

The views expressed are those of the author and are not necessarily those of Scientific American.

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  1. 1. dobermanmacleod 3:16 am 03/25/2013

    First, the Hayflick limit is the relatively new scientific discovery that human cells can only reproduce a set finite number of times. When our cells reach that limit, they become “zombie cells” (really) that basically sit there inflaming and toxifying the surrounding cells (making you look like h@ll, you know…like you’re a wrinkled prune aching all over).

    Check this out ( ), “experts” said there wasn’t a way to extend those telomere strands (you know the garbage DNA “caps” that are integral to cell reproduction and the avoidance of senescence), but now there is a least one proven product (TA-65, which cost about 400 $/month).

    This isn’t the magic bullet to avoid aging, since there are other animals who die without their telomere vanishing (lobster for one). Furthermore, because medical technology (like all technology) is increasing exponentially (not linearly like would be intuitive), it is likely that within twenty years there will be extreme longevity treatments that extend human life hundreds of years (for instance stem cell treatments, or longer term nanites in the body repairing DNA).

    Link to this
  2. 2. comfort 10:03 am 03/25/2013

    “Nobel Prize winner Elizabeth Blackburn is on this paper! No surprise there, telomeres are right up her alley!”

    No surprise, indeed. Blackburn seems to pop up on every kooky telomerase paper these days.

    This seems totally hand-waving. Enzyme production can go up for all sorts of reasons. Postulating an evolutionary adaptation here is pure speculation.

    Btw, dober, the Hayflick limit was described in 1961:
    Hayflick, L., and P. S. Moorhead. “The Serial Cultivation of Human Diploid Strains.” Exp. Cell Res. 25 (1961 1961): 585-621.

    Link to this
  3. 3. rshoff 11:57 am 03/25/2013

    So, we can infer that stressed out people may live longer while their happy stress-free counterparts succumb to prematurely running out of junk DNA… Sounds just.

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  4. 4. scicurious 12:01 pm 03/25/2013

    comfort: I wouldn’t call it handwaving. It’s certainly the first time anyone has looked at the effects of stress on telomerase activity, and it’s a logical step, esp in leucocytes (the cells they were looking at), given the effects of chronic stress on immune system function. They didn’t prove a mechanism, but they do not CLAIM to have proved a mechanism either. I also only speculated what this could mean, if it meant anything.

    rshoff: LOL, not just! To me it seems more likely (though they haven’t proven anything), that this is one protective mechanism against stress (of many mechanisms), but given the effects of stress that we still suffer from, it’s definitely not all that effective.

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  5. 5. rshoff 8:31 pm 03/25/2013

    @scicurious – Hey, let me have my fantasy! For once feel I may have an edge over my happy-go-lucky counterparts in life. ;-)

    But you would surely be proven right that the losses caused by stress are probably greater than the gains.

    The true benefit, of course, would be to keep people healthier throughout their nature life cycle -and perhaps extend it just a hair.

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  6. 6. comfort 8:29 am 03/26/2013

    I love your stuff, so consider me a friendly critic. But I do disagree here. The clear intent in both the article and your reporting is to imply that there *might* be a connection without any evidence that there *is* a connection. Call it hand-waving, call it hype, call it speculation–I find it pernicious, in light of the history of telomerase, in which people have long tried to sell both investors and the public on a link between cellular and organismal senescence that just isn’t demonstrated.

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  7. 7. scicurious 9:04 am 03/26/2013

    Comfort: hm. Justified criticism. I will add an edit.

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  8. 8. rshoff 12:01 pm 03/26/2013

    Aw, shucks.

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  9. 9. vincorine 6:12 pm 03/26/2013

    Does anybody worry about increased rates of cancer with increased telomerase activity? I seem to recall constitutive activity of telomerase as a hallmark of cancer cells. So, if stress does raise telomerase activity, does that increase the chances of cancer? Or would it only happen if the gene was permanently turned on?

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  10. 10. rshoff 1:55 pm 03/27/2013

    @vincorine – I’ve heard of the concept that if cells keep dividing indefinitely the cell line would accumulate DNA damage over time and eventually become cancerous (assuming cancer is the result of damaged DNA). But you mention cancer ‘rates’. The idea of increased cancer ‘rate’ implies to me that it’s not 100% so all immortal cell lines would not have to succumb to cancer. What would the increased rate be, and would it be low enough to be worth killing of a few cancerous cell lines from time to time? What are the mechanisms to repair damaged DNA?

    Perhaps reproduction is that mechanism. Reset the DNA to a clean(er) state for another generation. And evolve with the environment as it does. So much for the idea of ‘self’, but the DNA viability is preserved.

    Aha, the answer to the meaning of life, our raison d’être: preserve and enhance DNA.

    Just my thoughts. As you can tell I’m no scientist but I do get credit for caring to think about it and subscribing to SA. :-)

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  11. 11. JWilde 10:47 pm 05/7/2013

    An interesting article and interesting comments. Putting an end to telomere shortening would in fact be the magic bullet that would stop all aging. It is the sole mechanism that lies at the heart of aging in all species. It is the mechanism by which the species design of mortality is carried out. The mortal and immortal species on Earth can be divided precisely along the lines of those whose telomeres shorten and those that do not. Lobsters do not die of aging. What they do most often die of is a bit of a mystery – most likely starvation or inevitable predation brought on by their ever-increasing size. About the accumulating DNA damage, cells with telomeres that do not shorten – germ cells – do not suffer progressive DNA damage. If they did, every species would be quickly run into the ground by its own progressive DNA damage. In fact, each cell in our body is part of a 4-billion year lineage in which no DNA damage has accumulated because that trip was taken in the germ cell compartment. You can read more about the Lobster, the design of aging, and telomeres here

    Regards :)


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