EFFECT OF BENFOTHIAMINE AND ALPHA-LIPOIC ACID ON AUTONOMIC DYSFUNCTION IN TYPE 2 DIABETIC PATIENTS - PILOT STUDY
Objective: According to hypothesis that the lower level of bioactive thiamine, vitamin B1, is partially responsible for microvascular complications in type 2 diabetes patients (T2DM), we investigated whether the supplementation with benfothiamine and alpha-lipoic acid (ALA) could improve cardiac autonomic neuropathy (CAN) in those patients.
Research design and methods: Heart rate variability (HRV) was used as a tool for the assessment of equilibrium in the activity of the autonomic nervous system (ANS) in the control of heart rate in 8 T2DM patients, mean age 55.36 (4.63) years, with shorter duration of disease [median age 3 (interquartile range 2-3.5) years)] and the presence of metabolic syndrome (MeS), without serious co-morbidity. Ten healthy control subjects were also included in the study, age 48.50 (12.80) years. Blood samples for determining of the metabolic variables: glucose, HbA1c, triglycerides, cholesterol, and HDL-C were obtained from all patients before and at the end of treatment period. Patients were referred to Neurocardiology Unit and followed- up by the same examiner. For the evaluation of HRV, the time- and frequency domain analyses were used before and after treatment period (power spectral analysis).
Results: The ambulatory electrocardiogram (ECG) was recorded continuously for 24-hour. Mean high-frequency ln (HFln), was significantly lower (p< 0.01) and low- frequency/ high frequency ln (LF/HFln) was significantly higher (p<0.01) in T2DM, when compared with control subjects. After 12 weeks of treatment with benfothiamine and ALA, very low-frequency ln (VLFln), HFln and LF/HFln indices were corrected significantly (p=0.03; p=0.01; p=0.04, respectively). There were no significant changes for metabolic parameters or body mass index (BMI) during the study.
Conclusion: Our results demonstrated that benfothiamine associated with ALA could participate in repairing cardiac autonomic dysfunction in T2DM or made a shift of sympathovagal balance toward parasympathetic activation.