Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood. Proceedings of the National Academy of Sciences of the United States of America, 108(33), E513-E518

Department of Pediatrics, University of California, Irvine, CA 92697, USA.
Proceedings of the National Academy of Sciences (Impact Factor: 9.67). 08/2011; 108(33):E513-8. DOI: 10.1073/pnas.1107759108
Source: PubMed


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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    • "Their results indicate that at least anxiety symptoms may have a negative impact on TL. The authors argue that the physiological hyperarousal and physiological stress associated with anxiety disorders may cause telomere damage, consistent with other studies linking psychological stress with shorter TL (Ahola et al., 2012; Drury et al., 2012; 2014; Entringer et al., 2011; 2013; Epel et al., 2004; Humphreys et al., 2012; Kananen et al., 2010; O'Donovan et al., 2011; Price et al., 2013; Shalev et al., 2013a; Shalev et al., 2013b; Surtees et al., 2011; Tyrka et al., 2010; Uchino et al., 2012). On the other hand, there are also studies that do not support such an association, among them a most recent study assessing life stress in a 30-year birth cohort (Jodczyk et al., 2014; Phillips et al., 2013; Rius-Ottenheim et al., 2012). "
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    ABSTRACT: Shorter telomere length (TL) has found to be associated with lower birth weight and with lower cognitive ability and psychiatric disorders. However, the direction of causation of these associations and the extent to which they are genetically or environmentally mediated are unclear. Within-pair comparisons of monozygotic (MZ) and dizygotic (DZ) twins can throw light on these questions. We investigated correlations of within pair differences in telomere length, IQ, and anxiety/depression in an initial sample from Brisbane (242 MZ pairs, 245 DZ same sex (DZSS) pairs) and in replication samples from Amsterdam (514 MZ pairs, 233 DZSS pairs) and Melbourne (19 pairs selected for extreme high or low birth weight difference). Intra-pair differences of birth weight and telomere length were significantly correlated in MZ twins, but not in DZSS twins. Greater intra-pair differences of telomere length were observed in the 10% of MZ twins with the greatest difference in birth weight compared to the bottom 90% in both samples and also in the Melbourne sample. Intra-pair differences of telomere length and IQ, but not of TL and anxiety/depression, were correlated in MZ twins, and to a smaller extent in DZSS twins. Our findings suggest that the same prenatal effects that reduce birth weight also influence telomere length in MZ twins. The association between telomere length and IQ is partly driven by the same prenatal effects that decrease birth weight.
    Twin Research and Human Genetics 03/2015; 18(02):1-12. DOI:10.1017/thg.2015.3 · 2.30 Impact Factor
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    • "The elucidation of the mechanism underlying this relationship is still not clear. A finding from a human study has shown that prenatal stress leads to shorter leukocyte telomere length in adult offspring [59], which has also been found to positively correlate with the pathogenesis diabetes [60] and children obese [61]. "
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    ABSTRACT: Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.
    Journal of Diabetes Research 12/2013; 2013(1):485082. DOI:10.1155/2013/485082 · 2.16 Impact Factor
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    • "Maternal stress and maternal-placental-fetal biological mediators of stress can affect fetal development. In fact it has been showed that exposure to maternal psychosocial stress during intrauterine life is associated with significantly shorter leukocyte telomere length in young adulthood, a predictor of age related disease onset and mortality [62]. This provides a biological basis for speculation about the effects of early occurrence of poverty and how exposure to abuse, family conflict, emotional neglect and severe discipline could lead to individual differences in the nervous and endocrine response to stress and increase susceptibility to common adult disorders such as depression, anxiety, drug abuse or chronic diseases like diabetes, cardiovascular disease and obesity. "
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    ABSTRACT: According to the Barker hypothesis, the period of pregnancy and the intrauterine environment are crucial to the tendency to develop diseases like hypertension, diabetes, coronary heart disease, metabolic disorders, pulmonary, renal and mental illnesses. The external environment affects the development of a particular phenotype suitable for an environment with characteristics that closely resemble intrauterine conditions. If the extra-uterine environment differs greatly from the intra-uterine one, the fetus is more prone to develop disease. Subsequent studies have shown that maternal diseases like depression and anxiety, epilepsy, asthma, anemia and metabolic disorders, like diabetes, are able to determine alterations in growth and fetal development. Similarly, the maternal lifestyle, particularly diet, exercise and smoking during pregnancy, have an important role in determining the risk to develop diseases that manifest themselves both during childhood and particularly in adulthood. Finally, there are abundant potential sources of pollutants, both indoor and outdoor, in the environment in which the child lives, which can contribute to an increased probability to the development of several diseases and that in some cases could be easily avoided.
    Italian Journal of Pediatrics 01/2013; 39(1):7. DOI:10.1186/1824-7288-39-7 · 1.52 Impact Factor
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