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Using leukocyte telomere length as a biomarker of cellular aging, several studies have reported a significant correlation between personality traits and telomere length 3, 4, 5, 6. As such, telomere length may be considered as both a ‘mitotic clock’, reflecting cellular aging, and a mechanism through which age-related disease occurs 11, 12. Over time, progressively shortened telomeres may lead to cell-cycle arrest 8, apoptosis 9 or senescence 10. Crucial for the maintenance of genomic stability, telomeres protect against the attrition of genetic material, shortening with each cell division in most somatic tissues due to incomplete chromosome replication 7. Telomeres, tandem repeat guanine-rich DNA sequences, are specialised protective caps located at the ends of eukaryotic chromosomes. In an attempt to obtain a more objective measure of the impact of personality on aging, more recent research has examined the link between personality and telomere length 3, 4, 5, 6. While these studies support the role of personality in healthy aging 2, rather than measuring aging per se, many of these objective measures relate to symptoms of diseases or disorders with their own specific genetic and environmental risk factors. Recognising this limitation, some studies have focused on objective measures of aging including mortality, cardiovascular disease, immune function, or cancer. This means that much of the correlation between personality and healthy aging may not be causal, but instead could be explained by the reporting biases of individuals. However, the majority of studies of personality and aging have relied on self-report measures of symptoms, pain or physical functioning in old age. Multiple epidemiological studies report associations between personality traits such as dispositional optimism, anxiety or depression and (un)healthy aging in both cross-sectional and longitudinal designs 1, 2. These data support the hypotheses that an anxious predisposition contributes to accelerated telomere shortening in heart tissue, which may have important implications for our understanding of age-related heart disease, and that stress reactivity contributes to age-related telomere shortening in a tissue-specific manner. Telomere length was inversely related to stress reactivity in heart but not brain of aging individuals.
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We show that aging zebrafish have shorter telomeres in both heart and brain. Telomere length was assessed using quantitative PCR. Stress reactivity was assessed by tank diving and through gene expression. Here, we examined the correlation between stress reactivity and telomere length in heart and brain tissue in young (6–9 month) and aging (18 month) zebrafish. Thus, leukocyte telomere length may not accurately reflect telomere length in disease-relevant tissues. However, the effects of the HPA axis are tissue specific. Accelerated leukocyte telomere shortening is implicated in multiple age-related diseases and is associated with chronic activation of the hypothalamus–pituitary–adrenal (HPA) axis, providing a link between stress-related personality differences and adverse health outcomes. Health behaviours are often cited as the likely explanation for this association however, an underlying biological mechanism may also exist. Individual differences in personality are associated with variation in healthy aging.