Title: Allostatic Load and Epigenetic Age Acceleration in Early On-set Colorectal Cancer
The incidence rate of colorectal cancer (CRC) among all age groups combined has declined in recent decades, largely due to the increased uptake of CRC screening among eligible adults (≥45) and changes in lifestyle-related risk factors. Besides family history, established risk factors for CRC include age, inflammatory bowel disease, diabetes, alcohol consumption, smoking, red and processed meat intake, and sedentary lifestyle. Recent studies have shown that the accumulation of these known risk factors and potential novel risk factors (e.g., chronic stress) may accelerate biological aging, resulting in earlier susceptibility to cancer development. Indeed, when stratified by age, the incidence of early-onset CRC (EOCRC, <50) has risen by over 50% since the mid-1990’s. There is a need to find risk stratification biomarkers that can identify high-risk young adults who may benefit most from early CRC screening. Such novel biomarkers may include measures of chronic stress (i.e., allostatic load) and biological aging (i.e., epigenetic age acceleration), which may be more predominant in EOCRC vs. average-onset CRC etiology.
As an individual ages chronologically, their risk for age-related diseases (e.g., cancer) increases as a result of cumulative insults. A recent study reported the incidence of inherited cancer syndromes remain unchanged, thus implying that 80% of new EOCRC cases are sporadic, with no known family history. Temporal changes of known and/or novel lifestyle and environmental factors over the past several decades likely underscore the rise of sporadic EOCRC. For example, chronic stress changes DNA methylation patterns across the genome, impacting biological aging in various tissues (e.g., colon tissue). Epigenetic clocks were developed to capture this acceleration. Epigenetic age (EA), a biomarker, is the biological age of an individual as determined by DNA methylation levels across the genome. Epigenetic age acceleration (epiAA), the difference in chronological and epigenetic age, reflects the accumulation of insults - positive and negative effects of lifestyle and environmental factors - including chronic stress. Allostatic load (AL) is a cumulative measure of the physiological burden of chronic stress calculated from clinical biomarkers (e.g., blood pressure) and has been associated with an increased risk of many complex diseases. Although studies have shown that epiAA and AL are each associated with the increased risk of cancer, their interconnectedness and influence on EOCRC are less known. The goal of my research is to assess the translational potential of epiAA and/or AL as potential biomarkers for risk stratification and targeted screening for EOCRC.
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