ubiquinone and Depressive-Disorder

Most suicidality literature in Huntington disease (HD) is based on natural history studies or retrospective reviews, but reports on risk factors from clinical trials are limited.. We analyzed 609 participants from 2CARE, a randomized, double-blind, placebo-controlled clinical trial with up to 5 years of follow-up, for risk factors related to suicidality. The primary outcome variable was the time from randomization until the first occurrence of either suicidal ideation or attempt. We also considered time from randomization until the first suicide attempt as a secondary outcome variable.. These data suggest psychiatric comorbidities in HD are predictive of suicidal behavior while participating in clinical trials, reinforcing the importance of clinical surveillance and treatment towards lessening risk during participation and perhaps beyond. Designing a composite algorithm for early prediction of suicide attempts in HD may be of value, particularly given anticipated trials aimed at disease modification are likely to be long-term.. NCT00608881.

Topics: Adrenergic Uptake Inhibitors; Adult; Anti-Anxiety Agents; Antidepressive Agents; Anxiety Disorders; Bipolar Disorder; Depressive Disorder; Employment; Female; Humans; Huntingtin Protein; Huntington Disease; Male; Marital Status; Middle Aged; Randomized Controlled Trials as Topic; Risk Factors; Suicidal Ideation; Suicide, Attempted; Tetrabenazine; Trinucleotide Repeat Expansion; Ubiquinone; Vitamins

Amitriptyline is a commonly prescribed tricyclic antidepressant, which has been shown to impair mitochondrial function and increase oxidative stress in a variety of in vitro assays. Coenzyme Q(10) (CoQ(10)), an essential component of the mitochondrial respiratory chain and a potent antioxidant, has been proposed as a mitochondrial dysfunction marker. In order to evaluate the putative mitochondrial toxicity of amitriptyline, we have analyzed CoQ(10) and ATP levels, oxidative damage and mitochondrial mass in peripheral blood cells from control healthy volunteers and psychiatric patients with depressive episodes treated or non-treated with amitriptyline. In patients not following amitriptyline treatment, CoQ(10) and ATP levels and mitochondrial mass were reduced when compared to normal individuals while lipid peroxidation was clearly increased. All these alterations were aggravated in patients following oral amitriptyline therapy. These results suggest that mitochondrial dysfunction could be involved in the pathophysiology of depression and may be worsened by amitriptyline treatment. CoQ(10) supplementation is postulated to counteract the adverse effects of amitriptyline treatment in psychiatric patients.

Topics: Adenosine Triphosphate; Administration, Oral; Adult; Amitriptyline; Antidepressive Agents, Tricyclic; Antioxidants; Avitaminosis; Biomarkers; Depressive Disorder; Dietary Supplements; Female; Humans; Male; Mitochondria; Mitochondrial Diseases; Oxidative Stress; Ubiquinone

Topics: Adult; Antidepressive Agents; Benzoquinones; Brain; Depressive Disorder; DNA, Mitochondrial; Humans; Male; Point Mutation; Regional Blood Flow; RNA, Transfer; Tomography, Emission-Computed, Single-Photon; Ubiquinone