Field study reveals maternal age elevates chick corticosterone and reduces body mass in common gulls, suggesting endocrine-mediated reproductive senescence shapes offspring development.
Studying senescence in wild organisms reveals evolutionary trade-offs and life-history strategies that cannot be captured in laboratory settings. Long-lived seabirds from rare known-aged populations provide excellent models for examining aging under natural conditions. Because reproductive effort and self-maintenance are balanced throughout life, parental age can influence offspring phenotype through both genetic and non-genetic mechanisms. We investigated the effects of maternal and paternal age on offspring phenotype in the common gull ( Larus canus ), using known-aged breeders ranging from 3 to 18 years. We measured chick morphology (body size) and physiology, including corticosterone concentrations, telomere length, and immune parameters, in newly hatched chicks. Paternal age did not affect any offspring traits, whereas maternal age increased chick corticosterone concentrations, particularly in offspring of lower-quality females. Path analysis further showed that maternal age influenced chick body mass indirectly through corticosterone, suggesting that maternal senescence affects offspring quality via stress hormone–mediated pathways. These findings reveal sex-specific patterns of reproductive senescence in the wild, demonstrating that maternal—but not paternal—aging shapes offspring phenotype through endocrine mechanisms. Reduced growth in chicks of older, low-quality mothers may represent an adaptive adjustment to lower expected parental provisioning, resulting in development better matched to a constrained parental environment.
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Sepp et al. (2026) studied this question.
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