Maternal Stress Shortens Fetal Telomeres and Programs Aging and Disease In Utero

Maternal stress during pregnancy is associated with shorter telomeres in newborns, according to researchers at the Universities of California at Irvine and San Francisco, and the University of Pittsburgh.

Telomeres are short strands of DNA at the end of each chromosome that protect the chromosomes from deterioration or from fusing with other chromosomes. After each cell division, the telomeres become shortened and an enzyme known as telomerase adds more DNA to keep the telomeres intact. But over time, the telomeres reach a critical short length and the cell ages and dies. For this reason, telomere length has long been established as a marker for human aging – the shorter the telomeres, the earlier you will die.
Studies in the past few years have shown that the telomeres are far more than a marker for aging; they also mediate epigenetic changes, preserve the overall structure of chromatin (the DNA and proteins in the cell nucleus), and regulate gene expression. In effect, the telomere/telomerase system is one of the major mediators of health and disease throughout the lifespan.

A number of landmark studies have shown that psychological stress in adults is associated with shortening of the telomeres and accelerated aging. More recently, Sonja Entringer, Elissa Epel, and colleagues demonstrated that maternal psychological stress during pregnancy correlates with shorter telomeres in young adulthood. [1] Now they‘ve gone one step further to show that telomere shortening occurs in the fetus when the mother is psychologically stressed. [2] By measuring telomere length in leukocytes taken from the cord blood and assessing the mother‘s stress during her pregnancy, they were able to correlate the length of the telomeres with the degree of stress experienced by the mothers. In the words of the authors, ―it is plausible that in utero telomere biology represents a molecular mechanism whereby stress exposure in this critical period before birth can impact aging and subsequent disease susceptibility over the lifespan.

Short telomeres are also sign of oxidative stress in the womb, whether caused by maternal psychological stress or other stressors. In other words, womb stress causes senescence of fetal and placental tissues which can trigger preterm birth. One group at the University of Texas Medical Branch at Galveston correlated short fetal leukocyte telomere length with preterm prelabor rupture of the membranes and characterized the phenomenon as a ―placental membrane disease likely mediated by oxidative stress-induced senescence. [3]

Findings like this emphasize how important it is to reduce maternal stress during pregnancy and especially in the critical period before birth. Once the telomeres are shortened, the damage is done, although there have been promising attempts to stimulate telomerase activity in adults through mindfulness meditation and lifestyle factors such as a healthy diet and nurturing relationships. [4]

However, even if such efforts are proved to reduce negative effects of stress from the primal period, it is obviously much better to prevent that damage in the first place, especially since problems in early stages of development might easily lead to a cascade of further harmful consequences.

References

1. Entringer S, Epel ES, Kumsta R, et al. Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood. Proc Natl Acad Sci U S A. 2011;108(33):E513-8.
2. Entringer S, Epel ES, Lin J, et al. Maternal psychosocial stress during pregnancy is associated with newborn leukocyte telomere length. Am J Obstet Gynecol. 2013;208(2):134.e1-7.
3. Menon R, Yu J, Basanta-Henry P, et al. Short fetal leukocyte telomere length and preterm prelabor rupture of the membranes. PLoS One. 2012;7(2):e31136.
4. Daubenmier J, Lin J, Blackburn E, et al. Changes in stress, eating, and metabolic factors are related to changes in telomerase activity in a randomized mindfulness intervention pilot study. Psychoneuroendocrinology. 2012;37(7):917-28.