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Background
The purpose of this investigation was to examine heart rate variability (HRV), interbeat interval (IBI), and their interrelationship in healthy controls, bradycardic hyperpolarization‐activated cyclic nucleotide‐gated channel 4 (HCN4) mutation carriers, and patients with anorexia nervosa (AN). We tested the hypothesis that neural mechanisms cause bradycardia in patients with AN. Therefore, we assumed that saturation of the HRV/IBI relationship as a consequence of sustained parasympathetic control of the sinus node is exclusively detectable in patients with AN.
Methods
Patients with AN between the ages of 12 and 16 years admitted to our hospital due to malnutrition were grouped and included in the present investigation (N = 20). A matched‐pair group with healthy children and adolescents was created. Groups were matched for age and sex. A 24‐hour Holter electrocardiography (ECG) was performed in controls and patients. More specifically, all patients underwent two 24‐hour Holter ECG examinations (admission; refeeding treatment). Additionally, the IBI was recorded during the night in HCN4 mutation carriers (N = 4). HRV parameters were analyzed in 5‐minute sequences during the night and plotted against mean corresponding IBI length. HRV, IBI, and their interrelationship were examined using Spearman's rank correlation analyses, Mann‐Whitney U tests, and Wilcoxon signed‐rank tests.
Results
The relationship between IBI and HRV showed signs of saturation in patients with AN. Furthermore, signs of HRV saturation were present in two HCN4 mutation carriers. In contrast, signs of HRV saturation were not present in controls.
Conclusions
The existence of HRV saturation does not support the existence of parasympathetically mediated bradycardia. Nonneural mechanisms, such as HCN4 downregulation, may be responsible for bradycardia and HRV saturation in patients with AN.
(1) Background: Evidence has accumulated that patients with anorexia nervosa (AN) are at higher risk for vitamin D deficiency than healthy controls. In epidemiologic studies, low 25(OH) vitamin D (25(OH)D) levels were associated with depression. This study analyzed the relationship between 25(OH)D serum levels in adolescent patients and AN and depressive symptoms over the course of treatment. (2) Methods: 25(OH)D levels and depressive symptoms were analyzed in 93 adolescent (in-)patients with AN from the Anorexia Nervosa Day patient versus Inpatient (ANDI) multicenter trial at clinic admission, discharge, and 1 year follow up. Mixed regression models were used to analyze the relationship between 25(OH)D levels and depressive symptoms assessed by the Beck Depression Inventory (BDI-II). (3) Results: Although mean 25(OH)D levels constantly remained in recommended ranges (≥50 nmol/L) during AN treatment, levels decreased from (in)patient admission to 1 year follow up. Levels of 25(OH)D were neither cross-sectionally, prospectively, nor longitudinally associated with the BDI-II score. (4) Conclusions: This study did not confirm that 25(OH)D levels are associated with depressive symptoms in patients with AN. However, increasing risks of vitamin D deficiency over the course of AN treatment indicate that clinicians should monitor 25(OH)D levels.