Biological Ageing: A study of telomere length and mitochondrial DNA copy number in anorexia nervosa

Abstract

INTRODUCTION Patients with anorexia nervosa (AN) experience significant psychological and physical stress, which are risk factors for accelerated biological ageing. Telomeres are protective caps at the ends of chromosomes that prevent damage to the chromosome and preserve chromosomal integrity. Telomere length (TL) provides a measure of normal biological ageing and reduces with age. TL can also be reduced by stressors. Mitochondria, known as the "powerhouses" of the cell, are responsible for the production of energy. They are unique in that they possess their own DNA, distinct from nuclear DNA, of which there are many copies within the cell. Mitochondria may reflect stress via changes such as alterations in mitochondrial DNA copy number (mtDNAcn). I sought to test the following hypotheses: (1) TL is reduced in patients with AN compared to healthy controls; (2) TL is reduced with increasing duration and severity of illness; (3) mtDNAcn is increased in patients with AN compared to healthy controls; (4) mtDNAcn is increased with duration and severity of AN; and (5) mtDNAcn is correlated with TL. METHODS For this cross-sectional case control study, TL and mtDNAcn were assessed in peripheral whole blood DNA collected from patients with AN and age- and sex-matched healthy controls, using quantitative real-time polymerase chain reaction. Clinical and demographic characteristics were also obtained. Severity of illness was measured using the Eating Disorders Examination, a clinician-evaluated questionnaire. RESULTS Patients with AN (n=23; 21 females; mean age 30.3 years, SD 13.1) and age- and sex-matched controls (n=33; 32 females, mean age 30.6 years, SD 12.2) were included in the study. TL was significantly longer in patients with AN compared to healthy controls, both before and after adjusting for age, sex, level of educational attainment, smoking status, body mass index and antipsychotic use. TL was not associated with duration of illness after adjusting for age. TL was not associated with severity of illness. There was no difference between mtDNAcn in patients with AN compared to controls. mtDNAcn was positively associated with duration of illness, but not with illness severity. There was no correlation between TL and mtDNAcn. CONCLUSION Contrary to my hypotheses, the results indicate that TL does not reflect accelerated biological ageing in patients with AN. Further investigation may identify the reason for increased TL in those with AN. Interestingly, mtDNAcn was elevated in those with a longer duration of illness. Studies with larger sample sizes are required to clarify whether compensatory mechanisms increase mtDNAcn with increased illness duration.