ESPE Abstracts

Background: Small birth size followed by accelerated weight gain in early life is associated with an increased risk for age-associated diseases, such as cardiovascular disease (CVD) in later life. The underlying causes for this are largely unknown. Leukocyte telomere length (LTL) is a marker of biological age and short LTL is associated with increased CVD-risk. Subjects born small for gestational age (SGA) who remain short are treated with growth hormone (GH) to improve adult height.

Objective and hypotheses: To investigate whether birth size and adult body size, including spontaneous and GH-induced catch-up growth, influence LTL, hypothesizing that catch-up growth to a normal body size, either spontaneous or GH-induced, is associated with shorter LTL.

Method: We measured LTL in 558 young adults aged 18–24 years. LTL was measured using a quantitative PCR assay and expressed as T/S ratio. Using MR-analyses and by comparing clinically relevant subgroups, we analysed the influence of size at birth, adult body size, and GH-induced catch-up on LTL.

Results: We found no association between birth size and LTL. SGA born subjects with spontaneous catch-up to a normal body size had shorter LTL (3.07 (0.4)) than those born SGA who remained short (3.30 (0.4), p=0.003)) and appropriate for gestational age born subjects with a normal stature (AGA-NS) (3.22 (0.5), p=0.024)). The SGA-GH subgroup had a mean LTL of 3.27 (0.5), which was similar to LTL in the AGA-NS subgroup (p=0.74) and the short-SGA subgroup (p=0.73).

Conclusion: Birth size did not influence LTL. GH-treated young adults had similar LTL as subjects born AGA with a normal body size. Those born SGA with spontaneous catch-up in early life had the shortest LTL, suggesting that timing and tempo of early life growth influences telomere length, which could be one of the linkages between growth patterns and CVD-risk in later life.