Trina Aguirre

Background: Individuals with food addiction (FA) compose a distinct subset of people with obesity who are less responsive to weight loss interventions. An emerging field of study explores the role of telomere length in disease processes. Some evidence suggests that obesity is associated with telomere shortening; however, we are not aware of studies examining telomere length in obesity subtypes. Therefore, we explored whether FA and levels of obesity were associated with telomere shortening. Methods: We enrolled 120 adults (aged 19–70) with overweight/obesity (BMI ≥ 25); half were positive for severe food addiction (FA+), and half were negative for food addiction (FA−) (Yale Food Addiction Scale 2.0). Participants completed a demographic form and provided a saliva sample (Oragene saliva DNA collection kit). Telomere length was analyzed using the monoplex quantitative polymerase chain reaction (qPCR). Data were analyzed using descriptive statistics, t-tests, and ANOVAs (α = 0.05). Results: Participants with overweight (mean = 1.40 t/s, SD = 0.40) had longer telomeres (p = 0.013) than those with morbid obesity (mean = 1.15 t/s, SD = 1.29). Telomere length did not differ (p = 0.306) between persons who were FA− (mean = 1.26 t/s, SD = 0.26) and those who were FA+ (mean = 1.32 t/s, SD = 0.34). The youngest participants (mean = 1.39 t/s, SD = 0.33) had longer telomeres (p = 0.006) than the oldest participants (mean = 1.18 t/s, SD = 0.19). Conclusion: Those who were morbidly obese had the shortest telomere lengths. Interestingly, however, there were not significant telomere length differences in the food addicted vs. nonfood-addicted subtypes.