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Steve Pieczenik

Bio: Steve Pieczenik is an academic researcher. The author has contributed to research in topics: Menatetrenone & Dosing. The author has an hindex of 4, co-authored 13 publications receiving 687 citations.

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Journal ArticleDOI
TL;DR: Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat mitochondrial diseases and dysfunction, and antioxidant therapies hold promise for improving mitochondrial performance.

564 citations

Journal ArticleDOI
TL;DR: A review of the basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects can be found in this article, where the most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies.
Abstract: Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.

161 citations

01 Jan 2007
TL;DR: Cadmium, lead, and mercury have a minimum density of 5.1 and are defined in physiochemical terms as metals with a density at least 5 times as great as water as discussed by the authors.
Abstract: 1and are defined in physiochemical terms as metals with a density at least 5 times as great as water. This definition translates into an approximate heavy-metal minimum density of 5, and—in addition to cadmium, lead, and mercury—the metals zinc, copper, iron, cobalt, nickel, tin, manganese, and molybdenum also qualify. Scientifically, then, some heavy metals are essential nutrients. Cadmium (with a density of 8), lead (10), and mercury (14) are strikingly high in density compared with such common essential minerals as magnesium, calcium, or potassium, which all have densities below 2. Exposure to environmental contaminants comes through various routes, including natural sources (eg, groundwater, metal ores, and metal leaching from the soil), industrial processes, commercial products, and contaminated dietary supplements and food (eg, fish). 1 The risk for chronic toxicity depends on the frequency, intensity, and duration of contact with the contaminant along with the exposure route.

16 citations

01 Jan 2012
TL;DR: John Neustadt, ND, is medical director of Montana Integrative Medicine and president of Nutritional Biochemistry, Inc (NBI) in Bozeman.
Abstract: 4 Neustadt & Pieczenik—Preventing and Treating BRONJ John Neustadt, ND, is medical director of Montana Integrative Medicine and president of Nutritional Biochemistry, Inc (NBI) in Bozeman. Dr Neustadt has published more than 100 research reviews, is coauthor with Steve Pieczenik, MD, PhD, of the books A Revolution in Health Through Nutritional Biochemistry and Foundations and Applications of Medical Biochemistry in Clinical Practice.

2 citations


Cited by
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Journal ArticleDOI
TL;DR: Overall, this review outlines various mechanisms that lead to the development of oxidative stress and intervention and therapy that alter or disrupt these mechanisms may serve to reduce the risk of insulin resistance and theDevelopment of diabetes.

1,125 citations

Journal ArticleDOI
TL;DR: Myalgic encephalomyelitis: International Consensus Criteria (Review).
Abstract: 12 FatigueConsultationClinic,SaltLake RegionalMedicalCenter; 13 InternalMedicine,FamilyPractice,UniversityofUtah,SaltLakeCity,UT,USA; 14 ME ⁄CFSCenter,OsloUniversity HospitalHF,Norway; 15 DepartmentofPaediatrics,StateUniversityofNewYork,Buffalo,NY,USA; 16 Independent,Pavia,Italy; 17 Harbor-UCLA MedicalCenter,UniversityofCalifornia,LosAngeles,CA; 18 EVMedResearch,Lomita,CA,USA; 19 UniversityofLimerick,Limerick,Ireland; 20 Pain Clinic,KonyangUniversityHospital,Daejeon,Korea; 21 DonvaleSpecialistMedicalCentre,Donvale,Victoria,Australia; 22 Departmentsof Anesthesiology,NeurobiologyandAnatomy,UniversityofUtah,SaltLakeCity,UT,USA; 23 DepartmentofMedicinaNuclear,ClinicaLasCondes, Santiago,Chile; 24 WhittemorePetersonInstitute,UniversityofNevada,Reno,NV,USA; 25 MiwaNaikaClinic,Toyama,Japan; 26 A.Kirchenstein InstituteofMicrobiologyandVirology,RigaStradinsUniversity,Riga,Latvia; 27 DepartmentofBiochemistryBand 28 DepartmentofSportsSciences,UniversityofthePacific,Stockton,CAUSA

810 citations

Journal ArticleDOI
TL;DR: The purpose of the article is to highlight the recent progress on the mitochondrial role in metabolic syndromes and also summarize the progress of mitochondria-targeted molecules as therapeutic targets to treat metabolic Syndromes.

724 citations

Journal ArticleDOI
TL;DR: Evidence supports the notion that mitochondrial dysfunction is associated with autism spectrum disorders, and suggests children with ASD have a spectrum of mitochondrial dysfunction of differing severity.
Abstract: A comprehensive literature search was performed to collate evidence of mitochondrial dysfunction in autism spectrum disorders (ASDs) with two primary objectives. First, features of mitochondrial dysfunction in the general population of children with ASD were identified. Second, characteristics of mitochondrial dysfunction in children with ASD and concomitant mitochondrial disease (MD) were compared with published literature of two general populations: ASD children without MD, and non-ASD children with MD. The prevalence of MD in the general population of ASD was 5.0% (95% confidence interval 3.2, 6.9%), much higher than found in the general population (≈ 0.01%). The prevalence of abnormal biomarker values of mitochondrial dysfunction was high in ASD, much higher than the prevalence of MD. Variances and mean values of many mitochondrial biomarkers (lactate, pyruvate, carnitine and ubiquinone) were significantly different between ASD and controls. Some markers correlated with ASD severity. Neuroimaging, in vitro and post-mortem brain studies were consistent with an elevated prevalence of mitochondrial dysfunction in ASD. Taken together, these findings suggest children with ASD have a spectrum of mitochondrial dysfunction of differing severity. Eighteen publications representing a total of 112 children with ASD and MD (ASD/MD) were identified. The prevalence of developmental regression (52%), seizures (41%), motor delay (51%), gastrointestinal abnormalities (74%), female gender (39%), and elevated lactate (78%) and pyruvate (45%) was significantly higher in ASD/MD compared with the general ASD population. The prevalence of many of these abnormalities was similar to the general population of children with MD, suggesting that ASD/MD represents a distinct subgroup of children with MD. Most ASD/MD cases (79%) were not associated with genetic abnormalities, raising the possibility of secondary mitochondrial dysfunction. Treatment studies for ASD/MD were limited, although improvements were noted in some studies with carnitine, co-enzyme Q10 and B-vitamins. Many studies suffered from limitations, including small sample sizes, referral or publication biases, and variability in protocols for selecting children for MD workup, collecting mitochondrial biomarkers and defining MD. Overall, this evidence supports the notion that mitochondrial dysfunction is associated with ASD. Additional studies are needed to further define the role of mitochondrial dysfunction in ASD.

665 citations

Journal ArticleDOI
TL;DR: Statin administration is accompanied by risk reduction in all major vascular events in patients with CKD that are considered high-risk patients, and beneficial effects seem to be consequence of not only their hypolipidemic effect but especially their pleitropic actions that involve modulation of oxidative stress and inflammation.

529 citations