Born to Be Young?

Mom's prenatal thyroid hormones influence an infant's biological 'age' at birth...

Telomeres normally shorten as we age, indicating a higher incidence of disease along with higher mortality risk. Prenatal exposure to maternal stress hormones during embryo development, has previously been found to result in shorter telomeres and accelerates cell ageing.

"The telomere biology in humans is closer to the telomere biology in birds - than to other traditional laboratory animal models. In both humans and birds, telomere length is measured in a minimally-invasive way using small blood samples."

Antoine Stier PhD, Turku Collegium, University of Turku (Finland) and main author of the published research.

"Based on the natural decline in telomere length observed with age in the Collared Flycatcher bird population, we estimate chicks hatching from thyroid hormone injected eggs - were approximately 4 years 'younger at birth' than chicks hatched from control eggs."

Suvi Ruuskanen PhD, Turku Collegium, University of Turku (Finland).

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Although the underlying molecular mechanisms of such effects remain to be discovered, these new findings suggest prenatal thyroid hormones might have a role in setting individual 'biological age' at birth.

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"Considering controversies surrounding gene therapy trials in humans to elongate telomeres as an anti-ageing therapy — this discovery opens potential avenues to better understand the influence of telomere elongation using animal models."

Antoine Stier PhD.

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The study was conducted on a long-term monitored population of wild collared flycatcher breeding in Gotland island, and relied on extensive collaborations with the University of Uppsala (Sweden), Lyon, Glasgow and Aberdeen.

Abstract
The underlying mechanisms of the lifelong consequences of prenatal environmental condition on health and ageing remain little understood. Thyroid hormones (THs) are important regulators of embryogenesis, transferred from the mother to the embryo. Since prenatal THs can accelerate early-life development, we hypothesized that this might occur at the expense of resource allocation in somatic maintenance processes, leading to premature ageing. Therefore, we investigated the consequences of prenatal TH supplementation on potential hallmarks of ageing in a free-living avian model in which we previously demonstrated that experimentally elevated prenatal TH exposure accelerates early-life growth. Using cross-sectional sampling, we first report that mitochondrial DNA (mtDNA) copy number and telomere length significantly decrease from early-life to late adulthood, thus suggesting that these two molecular markers could be hallmarks of ageing in our wild bird model. Elevated prenatal THs had no effect on mtDNA copy number but counterintuitively increased telomere length both soon after birth and at the end of the growth period (equivalent to offsetting ca 4 years of post-growth telomere shortening). These findings suggest that prenatal THs might have a role in setting the ‘biological' age at birth, but raise questions about the nature of the evolutionary costs of prenatal exposure to high TH levels.

Authors
Antoine Stier , Bin-Yan Hsu , Coline Marciau , Blandine Doligez , Lars Gustafsson , Pierre Bize and Suvi Ruuskanen.

Acknowledgements
Published by the Royal Society. All rights reserved.

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