Telomeres are DNA/protein structures at the ends of chromosomes that shorten with age. Evidence is accumulating that telomere length is a biomarker of aging, providing a possible key towards understanding the enigma of aging, but the evidence is largely non-experimental. We will study telomeres in relation to aging and life history using an experimental approach in wild birds (jackdaws), which are exposed to natural selection pressures absent from laboratory settings. We have successfully modulated actuarial senescence (=increase of mortality rate with age) by inducing a change in reproductive effort through brood size manipulation, i.e. decreasing or increasing the number of young in the nest. This experiment also affected nestling development, but in a sex-dependent way: growth of daughters was more affected than growth of sons, but only in sons was there an effect on telomeres. Furthermore, the telomere shortening in nestlings was fast enough to allow longitudinal comparisons within weeks, while in humans this takes years. These findings create a unique opportunity to simultaneously test: (i) Whether the induced acceleration of actuarial senescence can be attributed to accelerated physiological aging, using telomere shortening as biomarker. (ii) Whether telomere dynamics in nestlings constitutes a biomarker that links developmental conditions to success later in life, and how this depends on sex. (iii) Candidate physiological causes of telomere shortening, exploiting the high rate of telomere shortening in nestlings. Through this experimental work in an ecologically relevant setting we will make a unique contribution to our understanding of telomeres, life histories and aging.