Telomeres Show Signs of Early-Life Stress

Reduction in telomere length is associated with stress early on in life and may have a genetic component, researchers find.

By | April 7, 2014

Chromosomes in metaphase with telomeric DNA stained red.WIKIMEDIA, ASAKO NAKAMURA ET AL.Telomere length in children is associated with a stressful home environment, and genes that encode certain neurotransmitters may heighten the effect of that stress, according to a study published today (April 7) in PNAS. Researchers led by Daniel Notterman of Pennsylvania State University studied 40 African American boys who were part of a large ongoing study of family stability, finding that children living in the most stressful environments had telomeres that were on average 40 percent shorter than those of the children studied who were living in the most nurturing settings. The researchers also found that those differences were exacerbated by variants in genetic pathways related to dopamine and serotonin production.

“I’m not surprised we found such a relationship and I’m not surprised by the gene interaction,” said Notterman. “I’m surprised by the magnitude of the association.”

Telomeres are long repetitive regions of nucleotides at the end of each chromosome. Along with the enzyme telomerase, they protect the ends of chromosomes from degrading or fusing with other chromosomes. Most studies that seek to evaluate the effects of stress on child development involve adults recalling their early-life memories. An ongoing study of the effect of family structure on childhood development—the Fragile Families and Child Wellbeing Study—provided the Penn State team with an opportunity to study the effects of stress on telomere length in children, and in real time. Fragile Families and Child Wellbeing Study participants were recruited at birth between 1998 and 2000 from 20 different U.S. cities.

For the present study, the researchers obtained DNA samples from 2,600 nine-year-old children. To avoid skewing their results with other factors that could affect telomere length, such as race and sex, the team only examined telomere length in African American boys.

The researchers further limited the study’s participants to those experiencing the most extreme levels of stress and nurturing. They rated each boy on several measures of early-life stress, such as economic status, parenting practices, and family stability, choosing 20 with the worst scores on these factors—excluding boys whose mothers had depression, which is linked to telomere length—and 20 with the most nurturing environments.

Despite the associations they observed, the researchers noted that it’s not yet clear whether early-life stress causes telomeres to shorten.

Even so, Notterman expressed hope that behavioral and social scientists hoping to link environmental and physiological factors might start also assessing telomere length. “The demonstration that telomere length is shortened by age nine supports the idea of early intervention,” Notterman said. Reduced telomere length is “not reversible as far as we know,” he added, and therefore “argues strongly for intervening early.”

But stress rarely affects people in the same way, noted Elissa Epel from the University of California, San Francisco, who was not involved in the research. “This study demonstrated this type of differential sensitivity to stress, based on genotype, with telomere shortening early in life,” Epel told The Scientist in an e-mail. “Although the sample is quite small, the data fits theory, and we should pay attention to this alarming story and extend it to other large samples when possible.”

Stacy Drury from the Tulane University School of Medicine in New Orleans, Louisiana, noted that gene-environment interactions may be at play. “My hope is that future studies are going to build upon this in a way that goes after really validated epistatic interaction, looking for an understanding of how these genes are actually biologically involved in this process,” she said.

Notterman’s team is extending its study of telomere length, and is in the process of taking repeat DNA samples from the participants, who are now 15 years old.

C. Mitchell et al., “Social disadvantage, genetic sensitivity and children’s telomere length,” PNAS, doi:10.1073/pnas.1404293111, 2014.

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Avatar of: EvMedDr


Posts: 14

April 8, 2014

This is yet another important observation that stress is a key modifier of biologic principles, both short- and long-term; indeed, physiologic stress may be the ultimate driver of Evolution. This observation of the association between stress and telomere length is complemented by another recent study showing the epigenetic inheritance of stress-induced behavior in mice. I fully agree with Stacy Drury's comment that we need to ultimately understand how the genes involved in this mechanism mediate the processes involved.

Avatar of: copernicus


Posts: 10

April 8, 2014

I posted this on another related item about how temperature affects the ability to resist cancer..., but it applies here as well, so there will be a few added edits.

It's not just about Social disadvantage and genetic sensitivity. There is a huge raft of stressors that affect epigenetic regulation.

"...but nobody ever thought to look" is the statement of importance here.

Here are a few other things, out of a long possible list, that they "never thought to look" a:

1) natural nutrition versus fast-foods.

2) constant ultrasounds, and other invasive procedures as per the human pregnancy "management". The problem there is that they can't mimic the psychological stress that the aggressive medical model of pregnancy management imposes on a human mother, which - like infections, initiates a cytokine response which also affect the foetus.

3) serial vaccines within a time appropriate frame, to both mothers and baby mice, mimicking the phenomenal immune stress imposed on human neonates through maternal and neonatal activation of cytokine pathways, which should be in a constant anti-inflammatory phenotype - not being forced to regularly shift to a pro-inflammatory phenotype.

You can't assume only things outside the medical model are relevant.

4) The differences in the immune systems comparing mouse-milk fed babies versus formula fed mouse babies.

5) The effects on the mouse micro biome of replicating the current completely irresponsible attitudes of the medical model in pregnancy and neonatal medicine of regularly napalming the body flora.

We already know that the immune systems of germ-free baby mice, kept germ free until adulthood, do not return to normal when "conventionalised" with good flora.

There is an immune system programming dependant upon that flora not being disturbed.

The medical literature shows there is ONE window of opportunity to get it "right" and if you fail, then everything else falls apart too.

It's not just "poverty" and "disadvantage" which is the main driver.

It's interesting how researchers constantly ignore how the medical model now imposes a ridiculously high level of physiological stressors on mothers and neonates.

That too is a stress which can shorten telomeres and cause non-infectious inflammatory epigenetic stress.

So there is another whole huge area that either "hasn't been thought of" or has been by-passed.

Who would want to look at the role the medical profession might play in creating problems?

Particularly if really studying daily life stressors imposed by the medical model on mothers and babies in early life...., might have funding repercussions.

Why are scientists always assuming that the main stressors are to be found outside of themselves? And why are scientists always assuming that they would be easily fixed by themselves?

Start asking HUMAN mothers what the biggest stresses being placed in them and their children are, and then scientists will be forced to look at the three fingers pointing at them, while they point one finger at families and the environment.

Avatar of: woody1217


Posts: 1

July 16, 2014

Stress will prove to be the most serious of our manageable illnesses.

Avatar of: PRice


Posts: 9

February 14, 2015

I found several questionable areas in this study. The largest is the way the researchers arrived at the concluding sentence, “We suggest that an individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.” They deliberately skewed the experimental 40-person sample, then made “findings” by pretending that contrasting two 20-person skewed samples of 9-year old boys represented something about stress and genetics in a larger population of children without proving their case.

Researchers cannot validly do this in children’s brain studies, for a comparable example. It is well known that long-term stress causes a child’s brain to develop differently than an unstressed child’s brain.

Further, instead of establishing a control group, the researchers split their sample according to maternal depression, which is an experimentally proven contributor to epigenetic changes detrimental to a developing fetus and on to infancy and early childhood. There are dozens of studies on that subject from which to choose on

So, of course, in general “ individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.” But the researchers didn’t do the work to find out whether it was the genetic architecture that the 9-year-olds were epigenetically changed into, or the genetic architecture they were conceived with, that stored the damage. I presume that this additional work wasn’t pursued because those type of findings wouldn’t make the race-baiting headlines of the press coverage this study was designed for.

Which leads me to ask – Was this study published to further an agenda other than make a contribution to science?

If so, does this study also represent a failure of the peer review process? Were the reviewers even interested in advancing science?


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