Very long chain fatty acids are an important marker of nutritional status in patients with anorexia nervosa: a case control study

BACKGROUND: Anorexia nervosa (AN) is a disease resulting in extreme weight loss. It is caused by multiple factors, including psychosocial, environmental, and genetic factors. A genetic abnormality affecting lipid metabolism has been recently reported in patients with AN. However, it is unknown whether lipid metabolism abnormalities in AN are caused by eating behavior, undernutrition, and/or genetic factors. The meaning of lipid metabolism in AN remains unclear. In particular, differences in the profiles of very long-chain fatty acids (VLCFAs) in patients with various types of AN have not been studied. This study aimed to determine changes to the fatty acid profile over a 3-month period, specifically that of long-chain fatty acids (LCFAs) and VLCFAs in patients with various types of AN. METHODS: We evaluated 69 female patients with AN, subclassified as AN-restricting type (AN-R) and AN-Binge-Eating/Purging type (AN-BP). On admission and after 3 months of treatment, height, weight, body mass index, plasma and serum parameters, and plasma fatty acid concentrations were measured in all patients. The control group included 25 healthy, age-matched women. Comparisons between the groups were made using one-way ANOVA, while those between the various parameters at admission and after 3 months within each group were made using the Wilcoxon signed rank test. RESULTS: On admission, the AN-R and the AN-BP groups had significantly higher levels of 18-24C and > 14C fatty acids (LCFAs and VLCFAs, respectively) than the control group. After 3 months of treatment, both groups showed high levels of 14-24C fatty acids. The levels of VLCFAs (C22:0 and C24:0) and LCFA (C18:3) after 3 months of treatment remained high in both AN groups relative to the control group. CONCLUSIONS: Eating behaviors appear to be associated with levels of LCFAs. Lipid metabolism abnormalities under conditions of starvation in AN might have a genetic basis and appear to be associated with VLCFA (C22:0 and C24:0) and LCFA (C18:3) levels.