Abstract
Aging populations face diminishing quality of life due to increased disease and morbidity. These challenges call for longevity research to focus on understanding the pathways controlling healthspan. We use the data from the UK Biobank (UKB) cohort and observe that the risks of major chronic diseases increased exponentially and double every eight years, i.e., at a rate compatible with the Gompertz mortality law. Assuming that aging drives the acceleration in morbidity rates, we build a risk model to predict the age at the end of healthspan depending on age, gender, and genetic background. Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan at the whole-genome significance level. We find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We thereby conclude that the healthspan offers a promising new way to interrogate the genetics of human longevity.
Highlights
Aging populations face diminishing quality of life due to increased disease and morbidity
We focused on aging and morbidity in mid-life using clinical histories for over 300,000 people, aged 37 to 73, and participating in the UK Biobank (UKB) cohort
We studied the dynamics of disease incidence using the clinical data available from the UKB
Summary
Aging populations face diminishing quality of life due to increased disease and morbidity. The increasing number of available genomes of very old people[7,8,9], though representing a rather specific and a relatively small sub-group of exceptionally successfully aging individuals, can provide an insight into the genetic architecture of exceptional life-spans and health-spans by use of Genome-Wide Association Studies (GWAS). While such studies suggested a fair number of loci, the APOE locus is probably among the few consistently implicated in multiple studies, see ref. We observed that the risk of the selected diseases increases exponentially at similar rates
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