Coenzyme Q10 Supplementation Research Articles

Effectiveness of combination therapy of magnesium, vitamin B2 and Co-enzyme 10 supplementation on vestibular migraine: a retrospective cohort study

Vestibular migraine (VM) has conventionally been treated through acute migraine-aborting therapeutic interventions and prevention to reduce migraines’ occurrence, length and intensity. There is growing attention to the development of non-pharmaceutical prophylactic interventions for migraines in the search for effective treatments, such as through mineral, vitamin and other supplementation. This research aims to examine the effectiveness of magnesium, vitamin B2 and Co-enzyme 10 supplementation to decrease vestibular migraines’ frequency, duration and severity. Method: This retrospective cohort study was conducted in a Jordanian context over 57- VM patients, each patient attending the outpatient dizziness clinic between August 2022 and February 2023. Patients were treated for six months with a combined supplementation of magnesium, vitamin B2, and Co-enzyme Q10. Assessments were made of three measures of VM attack, namely frequency, duration and severity, both before and after intervention. Result: Supplements administration demonstrated a significant reduction (by 81.1%) in VM-symptoms frequency (p < 0.001). Moreover, reductions in symptom duration in minutes occurred progressively as the treatment period continued and showed statistical significance, with impacts upon over 80% of the sample and a reduction from 763.9 minutes to 122.5 minutes (p < 0.001). The mean of pre-intervention severity was 7.2/10, with a significant decrease shown following treatment, at 2.1/10, and very positive results for over 71% of the sample (p < 0.001). Conclusion: The preliminary findings of this study showed a promising potential for such supplements in the treatment and prevention of VM; however, more research and a prospective trial are recommended.

Efficacy of coenzyme Q10 and curcumin on antioxidant enzyme activity and hippocampal alteration following exposure to cyclophosphamide in male rat

Coenzyme Q10 (KQ10) and curcumin (KUR) supplements are extensively used for their potential antioxidant, anticancer, and antiapoptotic properties. The present study investigated the neuroprotective potential of KQ10 and KUR against the side effect of cyclophosphamide (SF) (150mg/kg) on the hippocampus of male Wistar albino rats. Forty-nine 10–12 weeks old rats were randomly divided into seven groups: control, olive oil (OL), SF, KQ10, KUR, SF+KQ10, and SF+KUR. Our biochemical finding showed a significant decrease in superoxide dismutase (SOD) level in the SF group compared to the control group (p<0.05). There was also a significant reduction in the total number of the hippocampal pyramidal neurons in the CA1, CA2, and CA1-3 regions in the SF group compared to the control group (p<0.05). In the SF+KQ10 group, we found a significant increase in serum SOD level and the total number of the hippocampal pyramidal neurons in the CA1, CA2, and CA1-3 regions compared to the SF group (p<0.05). Immunohistochemical and histopathological examination exhibited noteworthy findings in the hippocampus tissues. Our findings showed that KQ10 administration significantly mitigated the hippocampal alteration caused by SF through enhancing antioxidant enzyme activity and reducing apoptosis. However, we found no protective activity of KUR on the hippocampus tissue, which may be due to its weak antioxidative activity.

Coenzyme Q10 mitigates macrophage mediated inflammation in heart following myocardial infarction via the NLRP3/IL1β pathway

BackgroundThe protective effect of Coenzyme Q10 (CoQ10) on the cardiovascular system has been reported, however, whether it can promote early recovery of cardiac function and alleviate cardiac remodeling after myocardial infarction (MI) remains to be elucidated. Whether CoQ10 may regulate the macrophage-mediated pro-inflammatory response after MI and its potential mechanism are worth further exploration.MethodsTo determine the baseline plasma levels of CoQ10 by LC-MS/MS, healthy controls and MI patients (n = 11 each) with age- and gender-matched were randomly enrolled. Additional MI patients were consecutively enrolled and randomized into the blank control (n = 59) or CoQ10 group (n = 61). Follow-ups were performed at 1- and 3-month to assess cardiac function after percutaneous coronary intervention (PCI). In the animal study, mice were orally administered CoQ10/vehicle daily and were subjected to left anterior descending coronary artery (LAD) ligation or sham operation. Echocardiography and serum BNP measured by ELISA were analyzed to evaluate cardiac function. Masson staining and WGA staining were performed to analyze the myocardial fibrosis and cardiomyocyte hypertrophy, respectively. Immunofluorescence staining was performed to assess the infiltration of IL1β/ROS-positive macrophages into the ischemic myocardium. Flow cytometry was employed to analyze the recruitment of myeloid immune cells to the ischemic myocardium post-MI. The expression of inflammatory indicators was assessed through RNA-seq, qPCR, and western blotting (WB).ResultsCompared to controls, MI patients showed a plasma deficiency of CoQ10 (0.76 ± 0.31 vs. 0.46 ± 0.10 µg/ml). CoQ10 supplementation significantly promoted the recovery of cardiac function in MI patients at 1 and 3 months after PCI. In mice study, compared to vehicle-treated MI mice, CoQ10-treated MI mice showed a favorable trend in survival rate (42.85% vs. 61.90%), as well as significantly alleviated cardiac dysfunction, myocardial fibrosis, and cardiac hypertrophy. Notably, CoQ10 administration significantly suppressed the recruitment of pro-inflammatory CCR2+ macrophages into infarct myocardium and their mediated inflammatory response, partially by attenuating the activation of the NLR family pyrin domain containing 3 (NLRP3)/Interleukin-1 beta (IL1β) signaling pathway.ConclusionsThese findings suggest that CoQ10 can significantly promote early recovery of cardiac function after MI. CoQ10 may function by inhibiting the recruitment of CCR2+ macrophages and suppressing the activation of the NLRP3/IL1β pathway in macrophages.Trial registrationDate of registration 09/04/2021 (number: ChiCTR2100045256).

The effects of coenzyme Q10 supplementation on biomarkers of exercise-induced muscle damage, physical performance, and oxidative stress: A GRADE-assessed systematic review and dose-response meta-analysis of randomized controlled trials

PurposeThis study aims to elucidate the dose-dependent effect of coenzyme Q10 supplementation (CoQ10) on exercise-induced muscle damage (EIMD), physical performance, and oxidative stress in adults. MethodsA systematic search was conducted through PubMed, Scopus, and ISI Web of Science databases up to August 2023, focusing on randomized control trials (RCTs) that investigated the effects of CoQ10 supplementation on EIMD recovery, physical performance and oxidative stress mitigation in adults. The weighted mean difference (WMD) and 95% confidence interval (95%CI) were estimated using the random-effects model. ResultsThe meta-analysis incorporated 28 RCTs, encompassing 830 subjects. CoQ10 supplementation significantly decreased creatine kinase (CK) (WMD: -50.64 IU/L; 95%CI: -74.75, -26.53, P<0.001), lactate dehydrogenase (LDH) (WMD: -52.10 IU/L; 95%CI: -74.01, -30.19, P<0.001), myoglobin (Mb) (WMD: -21.77 ng/ml; 95%CI: -32.59, -10.94, P <0.001), and Malondialdehyde (MDA) (WMD: -0.73 μmol/l; 95%CI: -1.26, -0.20, P =0.007) levels. No significant alteration in total antioxidant capacity was observed post-CoQ10 treatment. Each 100 mg/day increase in CoQ10 supplementation was correlated with a significant reduction in CK (MD: -23.07 IU/L, 95%CI: -34.27, -11.86), LDH (WMD: -27.21 IU/L, 95%CI: -28.23, -14.32), Mb (MD: -7.09 ng/ml; 95%CI: -11.35, -2.83) and MDA (WMD: -0.17 μmol/l, 95%CI: -0.29, -0.05) serum levels. Using SMD analysis, "very large" effects on LDH and "moderate" effects on CK and MDA were noted, albeit nonsignificant for other outcomes. ConclusionCoQ10 supplementation may be effective in reducing biomarkers of EIMD and oxidative stress in adults. Nevertheless, given the preponderance of studies conducted in Asia, the generalizability of these findings warrants caution. Further RCTs, particularly in non-Asian populations with large sample sizes and extended supplementation durations, are essential to substantiate these observations.

Optimizing Equilibration Protocols through Ubiquinone Supplementation in Goat Frozen Semen Diluent

The equilibration period is essential for sperm to adjust to the diluent, thereby preventing severe damage during cryopreservation. The elevation of lipid peroxidation during equilibration, indicating potential oxidative stress involvement, underscores the importance of optimizing equilibration protocols to minimize the detrimental effects of free radical production on sperm quality. This study aims to investigate the supplementation effect of adding ubiquinone to semen diluent on the membrane integrity, motility, and survivability of goat spermatozoa following an hour of equilibration. Ubiquinone supplementation was administered at varying doses: Group 2 (B) received 5 mg/dL, Group 3 (C) received 10 mg/dL, Group 4 (D) received 15 mg/dL, Group 5 (E) received 20 mg/dL, and Group 6 (F) received 25 mg/dL. Group A served as the negative control. Following one-way ANOVA examination of the research data, additional Duncan tests were conducted. The study results revealed that ubiquinone addition significantly (p&lt;0.05) affected the percentage of motility, viability, and membrane integrity of Kacang goat spermatozoa after one hour of equilibration. According to statistical analysis, the optimal concentration of ubiquinone in egg yolk skim milk to sustain motility is 12.5 mg/dL. Conversely, the most effective concentration for preserving the viability and membrane integrity of Kacang goat spermatozoa following equilibration is 25 mg/dL. In conclusion, the addition of ubiquinone to the frozen semen diluent maintains the stability of Kacang goat spermatozoa quality after equilibration.

The Spectrum of clinical manifestations in newborns with the COQ4 mutation: case series and literature review.

Coenzyme Q10 (CoQ10) plays an important role in the electron transport chain within the human mitochondrial respiratory chain. The manifestations of this deficiency exhibit a diverse range. This study investigates the clinical manifestations of primary coenzyme Q10 deficiency in neonates with the COQ4 mutation to improve the diagnosis of the disease and the prognosis through targeted treatment. We report 4 patients with primary coenzyme Q10 deficiency by COQ4 variants in neonates. A comprehensive literature search and review for original articles and case reports with COQ4 mutation published from January 1989 to November 2023 was performed through Pubmed. We review clinical manifestations, diagnostic approaches, and treatment monitoring in these and 20 previously reported patients. Within the cohort of four cases examined, three females and one male were identified from two distinct families. Specifically, case 1 and 2 consisted of monoamniotic twins. Cases 3 and 4 were siblings. A comprehensive review of 20 cases involving neonatal-onset COQ4 mutation was conducted. Half of the cases are Chinese. There was no statistically significant difference in the mortality between Chinese (9/12, 75%) and other regions (11/12, 91.7%) (P = 0.27). The survival time for the 24 cases was 60.0 ± 98.0 days (95% confidence interval CI: 0-252.0 days). The incidence of prenatal abnormalities in preterm infants was significantly higher than that in full-term infants (66.7% vs. 16.7%, P = 0.02). Hyperlactatemia was one of the most common manifestations, accounting for 75% of cases (18/24). Twenty of the 24 cases were diagnosed by whole exome sequencing. Only 9 patients received exogenous coenzyme Q10 treatment, and all the 4 surviving patients received coenzyme Q10 supplementation. The prognosis of COQ4 mutation in the neonatal period indicates a low survival rate and an poor prognosis. This may be due to the incomplete understanding of the mechanism of how COQ4 gene defects lead to coenzyme Q10 deficiency and why CoQ10 supplementation does not respond well to treatment. To improve the diagnostic rate, in addition to genetic testing, mitochondrial functional verification should be prioritized in southern China, where the incidence is relatively high. It will facilitate more in-depth mechanistic studies.

Mitochondrial Dysfunction and Coenzyme Q10 Supplementation in Post-Viral Fatigue Syndrome: An Overview.

Post-viral fatigue syndrome (PVFS) encompasses a wide range of complex neuroimmune disorders of unknown causes characterised by disabling post-exertional fatigue, myalgia and joint pain, cognitive impairments, unrefreshing sleep, autonomic dysfunction, and neuropsychiatric symptoms. It includes myalgic encephalomyelitis, also known as chronic fatigue syndrome (ME/CFS); fibromyalgia (FM); and more recently post-COVID-19 condition (long COVID). To date, there are no definitive clinical case criteria and no FDA-approved pharmacological therapies for PVFS. Given the current lack of effective treatments, there is a need to develop novel therapeutic strategies for these disorders. Mitochondria, the cellular organelles responsible for tissue energy production, have recently garnered attention in research into PVFS due to their crucial role in cellular bioenergetic metabolism in these conditions. The accumulating literature has identified a link between mitochondrial dysfunction and low-grade systemic inflammation in ME/CFS, FM, and long COVID. To address this issue, this article aims to critically review the evidence relating to mitochondrial dysfunction in the pathogenesis of these disorders; in particular, it aims to evaluate the effectiveness of coenzyme Q10 supplementation on chronic fatigue and pain symptoms as a novel therapeutic strategy for the treatment of PVFS.

Effects of coenzyme Q10 supplementation on oxidative stress biomarkers following reperfusion in STEMI patients undergoing primary percutaneous coronary intervention.

It is well-established that oxidative stress is deeply involved in myocardial ischemia-reperfusion injury. Considering the potent antioxidant properties of coenzyme Q10 (CoQ10), we aimed to assess whether CoQ10 supplementation could exert beneficial effects on plasma levels of oxidative stress biomarkers in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPIC). Seventy patients with the first attack of STEMI, eligible for PPCI were randomly assigned to receive either standard treatments plus CoQ10 (400 mg before PPCI and 200 mg twice daily for three days after PPCI) or standard treatments plus placebo. Plasma levels of oxidative stress biomarkers, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) were measured at 6, 24, and 72 hours after completion of PPCI. The changes in plasma levels of the studied biomarkers at 6 and 24 hours after PPCI were similar in the both groups (P values>0.05). This is while at 72 hours, the CoQ10- treated group exhibited significantly higher plasma levels of SOD (P value<0.001), CAT (P value=0.001), and TAC (P value<0.001), along with a lower plasma level of MDA (P value=0.002) compared to the placebo-treated group. The plasma activity of GPX showed no significant difference between the groups at all the study time points (P values>0.05). This study showed that CoQ10 has the potential to modulate the balance between antioxidant and oxidant biomarkers after reperfusion therapy. Our results suggest that CoQ10, through its antioxidant capacity, may help reduce the reperfusion injury in ischemic myocardium.

Mitochondrial electron transport chain, ceramide, and coenzyme Q are linked in a pathway that drives insulin resistance in skeletal muscle.

Insulin resistance (IR) is a complex metabolic disorder that underlies several human diseases, including type 2 diabetes and cardiovascular disease. Despite extensive research, the precise mechanisms underlying IR development remain poorly understood. Previously we showed that deficiency of coenzyme Q (CoQ) is necessary and sufficient for IR in adipocytes and skeletal muscle (Fazakerley et al., 2018). Here, we provide new insights into the mechanistic connections between cellular alterations associated with IR, including increased ceramides, CoQ deficiency, mitochondrial dysfunction, and oxidative stress. We demonstrate that elevated levels of ceramide in the mitochondria of skeletal muscle cells result in CoQ depletion and loss of mitochondrial respiratory chain components, leading to mitochondrial dysfunction and IR. Further, decreasing mitochondrial ceramide levels in vitro and in animal models (mice, C57BL/6J) (under chow and high-fat diet) increased CoQ levels and was protective against IR. CoQ supplementation also rescued ceramide-associated IR. Examination of the mitochondrial proteome from human muscle biopsies revealed a strong correlation between the respirasome system and mitochondrial ceramide as key determinants of insulin sensitivity. Our findings highlight the mitochondrial ceramide-CoQ-respiratory chain nexus as a potential foundation of an IR pathway that may also play a critical role in other conditions associated with ceramide accumulation and mitochondrial dysfunction, such as heart failure, cancer, and aging. These insights may have important clinical implications for the development of novel therapeutic strategies for the treatment of IR and related metabolic disorders.

Mitochondrial electron transport chain, ceramide, and coenzyme Q are linked in a pathway that drives insulin resistance in skeletal muscle

Insulin resistance (IR) is a complex metabolic disorder that underlies several human diseases, including type 2 diabetes and cardiovascular disease. Despite extensive research, the precise mechanisms underlying IR development remain poorly understood. Previously we showed that deficiency of coenzyme Q (CoQ) is necessary and sufficient for IR in adipocytes and skeletal muscle (Fazakerley et al., 2018). Here, we provide new insights into the mechanistic connections between cellular alterations associated with IR, including increased ceramides, CoQ deficiency, mitochondrial dysfunction, and oxidative stress. We demonstrate that elevated levels of ceramide in the mitochondria of skeletal muscle cells result in CoQ depletion and loss of mitochondrial respiratory chain components, leading to mitochondrial dysfunction and IR. Further, decreasing mitochondrial ceramide levels in vitro and in animal models (mice, C57BL/6J) (under chow and high-fat diet) increased CoQ levels and was protective against IR. CoQ supplementation also rescued ceramide-associated IR. Examination of the mitochondrial proteome from human muscle biopsies revealed a strong correlation between the respirasome system and mitochondrial ceramide as key determinants of insulin sensitivity. Our findings highlight the mitochondrial ceramide–CoQ–respiratory chain nexus as a potential foundation of an IR pathway that may also play a critical role in other conditions associated with ceramide accumulation and mitochondrial dysfunction, such as heart failure, cancer, and aging. These insights may have important clinical implications for the development of novel therapeutic strategies for the treatment of IR and related metabolic disorders.

Effects of L-Carnitine and Coenzyme Q10 Supplementation on Lower Urinary Tract Symptoms in Men with Benign Prostatic Hyperplasia: A Randomized, Controlled, Clinical Trial

The prevalence of benign prostatic hyperplasia (BPH) and its associated lower urinary tract symptoms (LUTS) increases with age. Considering that BPH drug treatment is associated with complications, this study aimed to investigate the effects of L-carnitine (LC) and Coenzyme Q10 (CoQ10) supplementation as an adjunct therapy to finasteride in the management of LUTS in older men affected with BPH. Fifty eligible volunteers (25 per group) were randomly assigned to either intervention (finasteride + LC and CoQ10 supplements) or control (finasteride + placebo) groups. International prostate symptom score (IPSS), international index of erectile function (IIEF), quality of life index (QoL), as well as serum levels of Prostate-specific antigen (PSA), were assessed. Prostate ultrasound evaluation was also performed, before and after 8 wk of intervention. Supplementation with LC and CoQ10 led to a significant decrease in prostate volume (p < 0.001) as well as a significant increase in IIEF (p < 0.001), compared to the control group. However, there were no significant between-group differences in IPSS (p = 0.503), QoL scores (p = 0.339), and PSA levels (p = 0.482). CoQ10 and LC supplements might be beneficial in combination with standard therapies in the management of BPH and its related complications.

Transcriptomic characterization of interactions between sodium selenite and coenzyme Q10 on preventing cadmium-induced testicular defects

The effect of heavy metal cadmium (Cd) on testicular function is recognized. However, the mechanism involved is not well-established. In the present study, we analyzed the testicular transcriptomic changes induced by acute Cd exposure of adult rats with and without supplementation of antioxidants selenium (Se) and/or coenzyme Q10 (CoQ). Cd significantly decreased serum testosterone and two steroidogenic proteins SCARB1 and STAR. RNA-Seq analyses of testicular RNAs revealed specific activation of oxidative stress-, inflammation-, MAPK- and NF-κB-related signaling molecules. In addition, Cd treatment down-regulated gene for I, III and IV complexes of mitochondrial electron transport chain and up-regulated genes for NADPH-oxidase, major cascade in ROS production. The decrease in steroidogenesis and increase in inflammation may result from oxidative stress since supplementation of Se and CoQ, but not with either alone, almost completely prevented these changes, including overall alterations in transcriptome. Cd exposure induced total of 1192 differentially expressed genes (DEGs), which was reduced to 29 without considering confounding factors associated with Se/CoQ, a 97.6% protection rate. In conclusion, Cd exposure inhibited Leydig cell steroidogenesis by down-regulating SCARB1 and STAR through increasing oxidative stress and inflammation, but Se plus CoQ synergistically prevented all the changes induced by the Cd exposure.

The Second Case of Bardet-Biedl syndrome from Iraq: An educational article and expert opinion

Background: Bardet-Biedl syndrome and Laurence-Moon syndrome are rare autosomal recessive disorders with a similar phenotype. They are characterized by the gradual development of phenotype which includes cone-rod retinal dystrophy, obesity, and hypogonadism in males. Other associated abnormalities include learning disability and renal abnormalities. The two conditions are differentiated clinically by the presence of spasticity and the absence of polydactyly in Laurence-Moon syndrome. In 2002, we reported the first patient with Bardet-Biedl syndrome. The boy had polydactyly, obesity, retinal degeneration, and was hospitalized at the University Hospital in Al-Kadhimiyia because of the development of chronic renal failure. Patients and methods: The case of a 9-year-old obese Kurdish girl who had polydactyly of the hands and feet associated with reduced visual acuity is described.Results: A 9-year-old obese Kurdish girl had polydactyly of the hand and feet associated with reduced visual acuity that was attributed to myopia which was partially corrected with eye glasses. The parents were unrelated, and her younger 5-year sister had polydactyly of the feet only. No other family member known to have polydactyly. Both sisters had their extra-digits removed surgically. The girl was studying at fourth grade primary school and the parents reported no learning disability. Fundoscopy showed normal optic disc and periphery of the retina. The presence of retinitis pigmentosa was excluded. However, the foveal reflex was reported to be abnormal by the oophthalmologist. Electroretinography showed evidence of cone-rod dystrophy.Conclusion: The second case of Bardet-Biedl syndrome from Iraq is reported. The current evidence-based expert opinion suggests the use of long tem supplementation of citicoline, co-enzyme Q10 and lutein with hope of retarding the progression to blindness.

Histological study on the toxic effect of titanium dioxide nanoparticles on the prostate gland of adult albino rats and the protective role of coenzyme Q10

Background Titanium dioxide nanoparticles have numerous clinical and commercial applications. Coenzyme Q10 has antioxidant and free radical-scavenging capabilities in addition to functions like vitamins. Aim To identify changes in the ventral prostatic lobe of adult albino rats exposed to titanium dioxide nanoparticles and to evaluate the possible protective role of coenzyme Q 10. Materials and methods Forty adult male albino rats were used in this study. Group I was the control, Group II received coenzyme Q10 at a dose of 20 mg/kg, Group III received titanium dioxide nanoparticles at a dose of 600 mg/kg, and Group IV received both coenzyme Q10 and nanoparticles. Prostate glands sections were stained with hematoxylin and eosin. A morphometric study and statistical analysis were performed on the epithelial height. Results Sections of group III showed some histological abnormalities in the form of widely spaced prostatic acini, an increase in the amount of connective tissue stroma, with numerous dilated blood vessels and perivascular cellular infiltration. The mean height of the prostatic epithelium in group III was significantly higher than in the control group. Prostatic epithelial height was found to be significantly lower in group IV as compared to group III. Conclusion Titanium dioxide nanoparticles induce changes in the prostatic ventral lobe which can be ameliorated by coenzyme Q10 supplementation.

Coenzyme Q10 Supplementation in Athletes: A Systematic Review.

To summarize available evidence in the literature on the impacts of CoQ10 supplementation on metabolic, biochemical, and performance outcomes in athletes. Six databases, Cochrane Library (33 articles), PubMed (90 articles), Scopus (55 articles), Embase (60 articles), SPORTDiscus (1056 articles), and Science Direct (165 articles), were researched. After applying the eligibility criteria, articles were selected for peer review independently as they were identified by June 2022. The protocol for this systematic review was registered on PROSPERO (CRD42022357750). Of the 1409 articles found, 16 were selected for this systematic review. After CoQ10 supplementation, a decrease in oxidative stress markers was observed, followed by higher antioxidant activity. On the other hand, lower levels of liver damage markers (ALT); Aspartate aminotransferase (AST); and Gamma-glutamyl transpeptidase (γGT) were identified. Finally, we found a reduction in fatigue indicators such as Creatine Kinase (CK) and an increase in anaerobic performance. This systematic review concludes that supplementation with orally administered CoQ10 (30-300 mg) was able to potentiate plasma antioxidant activity and anaerobic performance, reducing markers linked to oxidative stress and liver damage in athletes from different modalities aged 17 years old and older.

Royal Jelly Plus Ubiquinone Supplementation Improves Exercise Performance Through Attenuating Oxidative Stress In Female Swimmers

Royal Jelly Plus Ubiquinone Supplementation Improves Exercise Performance Through Attenuating Oxidative Stress In Female Swimmers

The Effect of Coenzyme Q10 as a Prophylactic Treatment in Episodic Migraine

Aim: Migraine is a neurological disorder characterized by recurring and often severe headaches. The aim of this study was to evaluate the effectiveness of coenzyme Q10 (CoQ10) in episodic migraine prophylaxis. Material and Methods: In a prospective follow-up study, 80 patients with episodic migraine were enrolled according to the International Classification of Headache Disorders 3rd edition and divided into two groups. One group consisted of 40 patients who received CoQ10 oral 200 mg twice daily as monotherapy for three months, while the other group consisted of 40 patients who received CoQ10 as an adjunct therapy in combination with other prophylactic antimigraine drugs. The Migraine Disability Assessment (MIDAS) questionnaire was administered to both groups before and after three months of therapy. Throughout the three-month therapy period, patients recorded daily symptoms, allowing for observation of changes in symptom severity, number, and duration of attacks from baseline. Results: Both groups that received CoQ10 supplementation exhibited positive responses. The group receiving adjunct therapy showed a statistically more significant reduction in the MIDAS (p&amp;lt;0.001), duration (p&amp;lt;0.001), and frequency (p&amp;lt;0.001) of attacks compared to the monotherapy group. Vomiting (p&amp;lt;0.001) in the adjunct therapy group completely disappeared and sound sensitivity (p=0.002) showed a dramatic response to treatment. Conclusion: CoQ10 appears to have more beneficial effects as an adjunct than monotherapy in reducing the duration, frequency, and presenting symptoms such as nausea, vomiting, and light sensitivity, in addition to sound sensitivity that responded only to adjunct therapy than monotherapy among Iraqi patients with episodic migraine.

Expanding the spectrum of neonatal-onset AIFM1-associated disorders.

Pathogenic variants in AIFM1 have been associated with a wide spectrum of disorders, spanning from CMT4X to mitochondrial encephalopathy. Here we present a novel phenotype and review the existing literature on AIFM1-related disorders. We performed EEG recordings, brain MRI and MR Spectroscopy, metabolic screening, echocardiogram, clinical exome sequencing (CES) and family study. Effects of the variant were established on cultured fibroblasts from skin punch biopsy. The patient presented with drug-resistant, electro-clinical, multifocal seizures 6 h after birth. Brain MRI revealed prominent brain swelling of both hemispheres and widespread signal alteration in large part of the cortex and of the thalami, with sparing of the basal nuclei. CES analysis revealed the likely pathogenic variant c.5T>C; p.(Phe2Ser) in the AIFM1 gene. The affected amino acid residue is located in the mitochondrial targeting sequence. Functional studies on cultured fibroblast showed a clear reduction in AIFM1 protein amount and defective activities of respiratory chain complexes I, III and IV. No evidence of protein mislocalization or accumulation of precursor protein was observed. Riboflavin, Coenzyme Q10 and thiamine supplementation was therefore given. At 6 months of age, the patient exhibited microcephaly but did not experience any further deterioration. He is still fed orally and there is no evidence of muscle weakness or atrophy. This is the first AIFM1 case associated with neonatal seizures and diffuse white matter involvement with relative sparing of basal ganglia, in the absence of clinical signs suggestive of myopathy or motor neuron disease.

Primary Coenzyme Q10 Deficiency: An Update

Coenzyme Q10 (CoQ10) has a number of vital functions in all cells, both mitochondrial and extra-mitochondrial. In addition to its key role in mitochondrial oxidative phosphorylation, CoQ10 serves as a lipid soluble antioxidant and plays an important role in fatty acid beta-oxidation and pyrimidine and lysosomal metabolism, as well as directly mediating the expression of a number of genes, including those involved in inflammation. Due to the multiplicity of roles in cell function, it is not surprising that a deficiency in CoQ10 has been implicated in the pathogenesis of a wide range of disorders. CoQ10 deficiency is broadly divided into primary and secondary types. Primary CoQ10 deficiency results from mutations in genes involved in the CoQ10 biosynthetic pathway. In man, at least 10 genes are required for the biosynthesis of functional CoQ10, a mutation in any one of which can result in a deficit in CoQ10 status. Patients may respond well to oral CoQ10 supplementation, although the condition must be recognised sufficiently early, before irreversible tissue damage has occurred. In this article, we have reviewed clinical studies (up to March 2023) relating to the identification of these deficiencies, and the therapeutic outcomes of CoQ10 supplementation; we have attempted to resolve the disparities between previous review articles regarding the usefulness or otherwise of CoQ10 supplementation in these disorders. In addition, we have highlighted several of the potential problems relating to CoQ10 supplementation in primary CoQ10 deficiency, as well as identifying unresolved issues relating to these disorders that require further research.

Effect of Coenzyme Q10 Supplementation on Middle Molecules in Hemodialysis Patients: A Randomized Clinical Trial

Background: Middle molecules, including some cytokines such as IL-6 and TNF-α, parathyroid hormone, etc., are types of uremic toxins having roles in the development of inflammation in hemodialysis patients. Different studies evaluating effects of coenzyme Q10 (CoQ10) on different inflammation markers in hemodialysis patients have controversial results. Moreover, no study determined the effect of CoQ10 on plasma concentration of IL-6, the most powerful predictor of poor outcomes and mortality, in hemodialysis patients. Therefore, a study was designed to examine the effects of CoQ10 supplementation on IL-6, TNF-α, and intact parathyroid hormone (iPTH) in chronic hemodialysis patients.&#x0D; Methods: In this single-blind randomized controlled trial, patients undergoing hemodialysis were randomly assigned to CoQ10 (100 mg/day) or control group. The duration of the study was 12 weeks. The plasma concentrations of IL-6, as the primary outcome, and TNF-α and iPTH, as the secondary outcomes, were measured at baseline and week 12.&#x0D; Results: Of 73 enrolled patients, 68 completed the study. At the end of the study, there were no significant differences in the concentrations of IL-6 (p=0.570), TNF-α (p=0.301), and iPTH (p=0.642) between the two groups. The standardized mean difference (CoQ10 vs. control) was -0.13 (95% CI -0.60; 0.35) for IL-6, -0.25 (95% CI -0.73; 0.22) for TNF-α, and 0.11 (95% CI -0.36; 0.59) for iPTH.&#x0D; Conclusion: This study showed a trivial effect of CoQ10 supplementation on the concentrations of IL-6 and iPTH and a small effect on the level of TNF-α in hemodialysis patients.