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Abstract
Leukocyte telomere length (LTL) is a complex genetic trait. It shortens with age and is associated with a host of aging-related disorders. Recent studies have observed that offspring of older fathers have longer LTLs. We explored the relation between paternal age and offspring's LTLs in 4 different cohorts. Moreover, we examined the potential cause of the paternal age on offspring's LTL by delineating telomere parameters in sperm donors. We measured LTL by Southern blots in Caucasian men and women (n=3365), aged 18–94 years, from the Offspring of the Framingham Heart Study (Framingham Offspring), the NHLBI Family Heart Study (NHLBI-Heart), the Longitudinal Study of Aging Danish Twins (Danish Twins), and the UK Adult Twin Registry (UK Twins). Using Southern blots, Q-FISH, and flow-FISH, we also measured telomere parameters in sperm from 46 young (<30 years) and older (>50 years) donors. Paternal age had an independent effect, expressed by a longer LTL in males of the Framingham Offspring and Danish Twins, males and females of the NHLBI-Heart, and females of UK Twins. For every additional year of paternal age, LTL in offspring increased at a magnitude ranging from half to more than twice of the annual attrition in LTL with age. Moreover, sperm telomere length analyses were compatible with the emergence in older men of a subset of sperm with elongated telomeres. Paternal age exerts a considerable effect on the offspring's LTL, a phenomenon which might relate to telomere elongation in sperm from older men. The implications of this effect deserve detailed study.
Highlights
Leukocyte telomere length (LTL) is a complex genetic trait
We examined by Q-FISH telomere length in subsets of sperm based on mitochondrial membrane potential (MMP), determined by 3,39-dihexyoxacarbocyanine iodide (DiOC6(3))
As the distributions were non-normal we examined the difference between sperm of older versus young donors in the median telomere length, which was significant
Summary
Leukocyte telomere length (LTL) is a complex genetic trait. Though highly variable, it is heritable [1,2,3,4,5,6] and longer in women than men [1,3,4,6,7,8,9]. The mechanisms that account for variations among humans in LTL are not fully understood, increased oxidative stress and inflammation – two potential determinants of life span and aging-related diseases [23,24] – are likely to heighten age-dependent telomere attrition in leukocytes [9,12,14, 25 reviewed in 26]. As aging-related diseases and environmental factors may cause premature mortality, and as men’s LTL [1,7,9,14,25] and life expectancy [27] are shorter than women’s, the potential relation between LTL and human longevity has been explored in several studies, which yielded conflicting results [18,28,29,30,31]
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