Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood
Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknow...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 108; no. 33; pp. E513 - E518 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
16.08.2011
National Acad Sciences |
| Series | PNAS Plus |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.1107759108 |
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| Abstract | Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. |
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| AbstractList | Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. [PUBLICATION ABSTRACT] Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk.Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. To summarize, this study provides evidence in humans that maternal psychosocial stress exposure during gestation is a significant predictor of the offspring's subsequent leukocyte telomere length, a marker of cellular aging, in young adulthood. This, in turn, suggests that the trajectory of cellular aging in humans may be influenced by stress in intrauterine life, thereby potentially increasing the susceptibility of prenatally stressed individuals for complex, common age-related diseases. Many questions remain concerning the exact mechanisms underlying prenatal programming of telomere length and the directionality of the associations among prenatal stress, telomere length, and later health outcomes. Nonetheless, this study represents an important step, and these results add further evidence to the growing awareness that disease pathways for complex, common age-related disorders may have their foundations very early in life. Our study has a few limitations. First, prenatal stress exposure was assessed retrospectively. Although retrospective assessments of psychosocial factors such as stress are prone to biases such as “after-the-fact” reporting (i.e., individuals who develop health disorders are more prone to retrospectively report higher levels of adverse exposures before the development of the disorder) and those produced by memory and current psychological state (affect/mood), we believe it is unlikely these biases significantly impacted our assessment of prenatal stress in the present study. All subjects were healthy young adults; they received identical information before and upon entering the study, they were not provided any information about the study hypotheses, and they (as well as the experimenters) were blinded to and had no a priori knowledge about the expected direction of study findings. Subjects in the two groups did not differ in their current baseline psychological state (depressive symptoms, perceived stress) or memory performance scores. Moreover, our use of major negative life events to retrospectively assess psychosocial stress exposure provides greater confidence for construct validity than would have been the case for retrospective assessments of other components of stress such as perceived severity of stress appraisals or stress symptoms. Second, men were underrepresented in our study. Some studies have reported sex-specific effects of prenatal stress exposure on certain outcomes. As the effect of prenatal stress on telomere length in the present study was largest in the women only group, this raises the intriguing possibility and speculation regarding potential sex-specific programming effects in this context. However, we did not have the statistical power to examine possible sex-specific programming effects. There are several pathways that may have led to the striking observation in the present study. Exposure to high levels of maternal stress during pregnancy is known to produce deleterious effects on the offspring's developing endocrine, immune, and metabolic systems, and our previously published studies in this cohort have reported that the prenatally stressed individuals exhibited alterations in several of these parameters, including higher stimulated levels of IL-6, a cytokine that has been directly associated with shorter telomere length. Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring ( Fig. P1 ). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, postnatal early-life adversity, and concurrent stress level), and was more pronounced in women. The magnitude of the observed difference in leukocyte telomere length between the prenatal stress exposure group and the comparison group is striking. The leukocyte telomere length of individuals in the prenatally stressed individuals was, on average, 178 bp shorter than that of individuals in the comparison group (and 295 bp shorter in female subjects). This effect equates to a difference of 0.41 SDs in telomere length in the prenatal stress exposure group relative to the comparison group (and 0.68 SDs in female subjects). Based on the most recent and comprehensive review of studies of age-related attrition in telomere length ( 4 ), translating telomere shortening of this observed difference to years of aging indicates that the leukocytes of individuals in the prenatal stress group aged the equivalent of approximately 3.5 additional years (5 additional years in the women-only group) relative to those in the comparison group. The objective of the present study was to test the hypothesis that maternal psychosocial stress exposure during pregnancy is associated with shorter telomeres in their offspring during adult life. Because it is not possible to randomly assign exposure to stress during human pregnancy, we approximated experimental exposure by enrolling young adults whose mothers happened to have experienced a high level of psychosocial stress during pregnancy (a major negative life event; the prenatal stress group) and comparing them with a group of subjects whose mothers had not been exposed to negative life events during pregnancy (comparison group). The potential confounding effects of other sociodemographic, obstetric, medical, and behavioral risk factors were addressed by using a stringent set of exclusionary criteria. Moreover, because prenatal stress exposure may be associated with subsequent conditions that may influence telomere length, such as presence of postnatal early-life adversity, inadequate parental care, or concurrent stress level, we assessed these constructs to statistically account for their possible confounding effects. A rapidly growing body of empirical evidence suggests that the origins of susceptibility for many common age-related disorders can be traced back to the intrauterine period of life (i.e., the concept of fetal, or developmental, origins of health and disease risk) ( 1 ). Exposure to psychosocial stress and/or biological stress mediators during gestation has been identified as one salient condition that may underlie the long-term effects of the intrauterine environment ( 2 ). The link between psychosocial stress exposure and adverse health outcomes is well established, and the elucidation of biological processes underlying this relationship is of ongoing interest. In recent years, accumulating evidence supports an important role for telomere biology as a potential mechanism linking stress and disease risk ( 3 ). Telomeres are DNA–protein complexes that cap chromosomal ends and promote chromosomal stability. They shorten in all replicating somatic cells, including white blood cells, with age and with conditions that produce oxidative stress. Declines in the telomere/telomerase maintenance system serve as a biomarker of cellular integrity and likely play a causal role in aging. One important question that has yet to be addressed is whether exposure to stress during intrauterine development can produce variations in telomere length, thereby potentially setting up a long-term trajectory at birth that contributes to individual susceptibility for age-related common diseases. Evidence linking other adverse conditions during fetal development (e.g., intrauterine growth restriction, poor maternal nutrition during pregnancy) with telomere length provides biological plausibility for this relationship. Leukocyte telomere length (LTL) is a predictor of age-related disease onset and mortality. The association in adults of psychosocial stress or stress biomarkers with LTL suggests telomere biology may represent a possible underlying mechanism linking stress and health outcomes. It is, however, unknown whether stress exposure in intrauterine life can produce variations in LTL, thereby potentially setting up a long-term trajectory for disease susceptibility. We, therefore, as a first step, tested the hypothesis that stress exposure during intrauterine life is associated with shorter telomeres in adult life after accounting for the effects of other factors on LTL. LTL was assessed in 94 healthy young adults. Forty-five subjects were offspring of mothers who had experienced a severe stressor in the index pregnancy (prenatal stress group; PSG), and 49 subjects were offspring of mothers who had a healthy, uneventful index pregnancy (comparison group; CG). Prenatal stress exposure was a significant predictor of subsequent adult telomere length in the offspring (178-bp difference between prenatal stress and CG; d = 0.41 SD units; P < 0.05). The effect was substantially unchanged after adjusting for potential confounders (subject characteristics, birth weight percentile, and early-life and concurrent stress level), and was more pronounced in women (295-bp difference; d = 0.68 SD units; P < 0.01). To the best of our knowledge, this study provides the first evidence in humans of an association between prenatal stress exposure and subsequent shorter telomere length. This observation may help shed light on an important biological pathway underlying the developmental origins of adult health and disease risk. |
| Author | Kumsta, Robert Hellhammer, Dirk H Wadhwa, Pathik D Wüst, Stefan Entringer, Sonja Epel, Elissa S Blackburn, Elizabeth H Lin, Jue |
| Author_xml | – sequence: 1 fullname: Entringer, Sonja – sequence: 2 fullname: Epel, Elissa S – sequence: 3 fullname: Kumsta, Robert – sequence: 4 fullname: Lin, Jue – sequence: 5 fullname: Hellhammer, Dirk H – sequence: 6 fullname: Blackburn, Elizabeth H – sequence: 7 fullname: Wüst, Stefan – sequence: 8 fullname: Wadhwa, Pathik D |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21813766$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Adult adulthood Adults Age Biological Sciences biomarkers birth weight Case-Control Studies Chromosomes disease resistance Exposure Female Health risks Humans Infant, Newborn Intrauterine devices IUD Leukocytes Male mortality mothers Mothers - psychology Offspring PNAS Plus Pregnancy Pregnancy Complications - psychology Prenatal Exposure Delayed Effects progeny Risk Stress Stress, Psychological Telomere telomeres women Young Adult Young adults |
| Title | Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood |
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