ABSTRACT
BACKGROUND: Bipolar disorder may be associated with mitochondrial dysfunction. Therefore, agents that enhance mitochondrial functioning may be efficacious in bipolar disorder. We performed a randomized placebo-controlled trial of the mitochondrial enhancers acetyl-L-carnitine (ALCAR) and α-lipoic acid (ALA) in patients with bipolar depression, and assessed markers of cerebral energy metabolism using phosphorus magnetic resonance spectroscopy. METHODS: We administered ALCAR (1000-3000 mg daily) plus ALA (600-1800 mg daily) or placebo for 12 weeks to 40 patients with bipolar depression and obtained imaging data at baseline, week 1, and week 12 of treatment in 20 patients using phosphorus 3-dimensional chemical-shift imaging at 4 T. Statistical analysis used random effects mixed models. RESULTS: We found no significant difference between ALCAR/ALA and placebo on change from baseline in the Montgomery-Asberg Depression Rating Scale in both the longitudinal (mean difference [95% confidence interval], -1.4 [-6.2 to 3.4], P = 0.58) and last-observation-carried-forward (-3.2 [-7.2 to 0.9], P = 0.12) analyses. ALCAR/ALA treatment significantly reduced phosphocreatine levels in the parieto-occipital cortex at week 12 (P = 0.002). Reduction in whole brain total nucleoside triphosphate levels from baseline to week 1 was associated with reduction in Montgomery-Asberg Depression Rating Scale scores (P = 0.02) in patients treated with ALCAR/ALA. However, this was likely a chance finding attributable to multiple statistical comparisons. CONCLUSIONS: Treatment with ALCAR and ALA at the dose and duration used in this study does not have antidepressant effects in depressed bipolar patients and does not significantly enhance mitochondrial functioning in this patient group.
Subject(s)
Acetylcarnitine/therapeutic use , Antidepressive Agents/therapeutic use , Bipolar Disorder/drug therapy , Thioctic Acid/therapeutic use , Adult , Bipolar Disorder/diagnosis , Bipolar Disorder/metabolism , Bipolar Disorder/psychology , Brain/drug effects , Brain/metabolism , Chi-Square Distribution , Drug Therapy, Combination , Energy Metabolism/drug effects , Female , Humans , Linear Models , Magnetic Resonance Spectroscopy , Male , Middle Aged , Mitochondria/drug effects , Mitochondria/metabolism , Phosphocreatine/metabolism , Psychiatric Status Rating Scales , Time Factors , Treatment OutcomeABSTRACT
OBJECTIVE: To estimate how much the prevalence of binge eating disorder will increase under the new proposed DSM-5 criteria, which relax the requirements for the frequency and duration of eating binges. METHOD: Interview data from a nonclinical sample of 888 first-degree relatives who had participated in a family study of binge eating disorder were analyzed. The probands in this study (not included in this analysis) had been selected to either have binge eating disorder or no history of eating binges. RESULTS: The increase in the prevalence of binge eating disorder using the proposed DSM-5 criteria relative to the DSM-IV criteria was 2.9% in women and 3.0% men for lifetime prevalence, and 7.7% in women and 0% in men for the point prevalence. DISCUSSION: Changes in frequency and duration of binge episodes proposed for DSM-5 will likely have only a minimal effect on the prevalence of binge eating disorder.
Subject(s)
Binge-Eating Disorder/diagnosis , Binge-Eating Disorder/epidemiology , Diagnostic and Statistical Manual of Mental Disorders , Adult , Female , Humans , Male , PrevalenceABSTRACT
BACKGROUND: Binge-eating disorder may represent a risk factor for the metabolic syndrome. OBJECTIVE: The objective was to assess longitudinally the relation between binge-eating disorder and components of the metabolic syndrome. DESIGN: At 2.5 and 5 y of follow-up, 134 individuals with binge-eating disorder and 134 individuals with no history of eating disorders, who were frequency-matched for age, sex, and baseline body mass index (BMI), were interviewed during the follow-up interval regarding new diagnoses of 3 metabolic syndrome components: hypertension, dyslipidemia, and type 2 diabetes. RESULTS: A comparison of individuals with and without a binge-eating disorder in analyses adjusted for age, sex, baseline BMI, and interval BMI change had hazard ratios (95% CIs) for reporting new diagnoses of metabolic syndrome components of 2.2 (1.2, 4.2; P = 0.023) for dyslipidemia, 1.5 (0.76, 2.9; P = 0.33) for hypertension, 1.6 (0.77, 3.9; P = 0.29) for type 2 diabetes, 1.7 (1.1, 2.6; P = 0.023) for any component, and 2.4 (1.1, 5.7; P = 0.038) for > or =2 components. CONCLUSION: Binge-eating disorder may confer a risk of components of the metabolic syndrome over and above the risk attributable to obesity alone. This trial was registered at www.clinicaltrials.gov as NCT00777634.
