Document Detail


Detection of metabolic syndrome in schizophrenia and implications for antipsychotic therapy : is there a role for folate?
MedLine Citation:
PMID:  23341251     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In general, the presence of metabolic syndrome is associated with significant cardiovascular mortality and represents a growing public health concern in the USA. Patients with schizophrenia have a three times greater risk of death than the general population, with cardiovascular disease being the most common cause of this mortality. Use of atypical antipsychotics (AAPs) to treat schizophrenia contributes significantly to this cardiovascular risk. While several different clinical guidelines currently exist to monitor the metabolic consequences of AAP use, implementation is lacking. Because of under-monitoring of side effects and the lack of alternative treatment choices in schizophrenia, research has focused on identification of various biomarkers and pharmacogenomic targets to focus on the patients at greatest risk of metabolic syndrome, thus aiming to increase the efficacy and minimize the side effects of AAPs. This has led to several different lines of research. This review focuses on summarizing the differing metabolic syndrome criteria, monitoring guidelines for use of AAPs, and the role of folic acid as it relates to metabolic syndrome within the schizophrenia population. It concentrates not only on the pharmacogenomics of folic acid metabolism but also on its epigenetic interaction with the environment. From this work, genetic variation within both the methylenetetrahydrofolate reductase (MTHFR) gene and the catechol-O-methyltransferase (COMT) gene has been associated with an increased risk of metabolic syndrome in schizophrenia patients treated with AAPs. Furthermore, work on the combination of folate pharmacogenetics and epigenetics has uncovered relationships between methylation, schizophrenia disease, treatment type, and metabolic syndrome. Despite several areas of biomarker research into schizophrenia-related metabolic syndrome, translation into the clinical setting is still lacking, and further studies are needed to bridge this gap. In the future, folate supplementation may prove to be an easy and effective clinical tool for prevention and/or treatment of metabolic syndrome associated with AAP treatment, but clearly more research needs to be done in this area.
Authors:
Kyle J Burghardt; Vicki L Ellingrod
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Molecular diagnosis & therapy     Volume:  17     ISSN:  1179-2000     ISO Abbreviation:  Mol Diagn Ther     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-06     Completed Date:  2013-08-09     Revised Date:  2014-07-02    
Medline Journal Info:
Nlm Unique ID:  101264260     Medline TA:  Mol Diagn Ther     Country:  New Zealand    
Other Details:
Languages:  eng     Pagination:  21-30     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Antipsychotic Agents / adverse effects*,  therapeutic use
Cardiovascular Diseases / etiology,  prevention & control
Catechol O-Methyltransferase / genetics,  metabolism
Dietary Supplements*
Epigenomics / methods
Folic Acid / administration & dosage*
Humans
Metabolic Syndrome X / complications,  drug therapy*
Methylenetetrahydrofolate Reductase (NADPH2) / genetics,  metabolism
Pharmacogenetics
Risk Factors
Schizophrenia / complications,  drug therapy*
Grant Support
ID/Acronym/Agency:
5P60 DK 20572/DK/NIDDK NIH HHS; K08 MH064158/MH/NIMH NIH HHS; K08 MH64158/MH/NIMH NIH HHS; M01 RR000059/RR/NCRR NIH HHS; R01 MH082784/MH/NIMH NIH HHS; R01 MH082784/MH/NIMH NIH HHS; UL1 RR024986/RR/NCRR NIH HHS; UL1RR024986/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antipsychotic Agents; 935E97BOY8/Folic Acid; EC 1.5.1.20/Methylenetetrahydrofolate Reductase (NADPH2); EC 2.1.1.6/Catechol O-Methyltransferase
Comments/Corrections

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