Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers
Background/Objectives: The objective of the study was to assess the role of variations in serum folate, vitamin B12, homocysteine and the presence of genetic polymorphisms as risk factors for congenital heart disease (CHD) in children. Subjects/Methods: A total of 32 children with CHD, and their mot...
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| Veröffentlicht in: | European journal of clinical nutrition 2017-12, Vol.71 (12), p.1437-1441 |
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| creator | Elizabeth, K E Praveen, S L Preethi, N R Jissa, V T Pillai, M R |
| description | Background/Objectives:
The objective of the study was to assess the role of variations in serum folate, vitamin B12, homocysteine and the presence of genetic polymorphisms as risk factors for congenital heart disease (CHD) in children.
Subjects/Methods:
A total of 32 children with CHD, and their mothers and 32 normal children and their mothers formed the study and control groups, respectively. Serum folate, vitamin B12 and homocysteine as well as genetic polymorphisms MTHFR C677→T, MTHFR A1298→C, MTR A2756→G and MTRR A66→G were assessed.
Results:
Low serum folate and genetic polymorphisms MTHFR C677→T and MTRR A66→G among children and their mothers and high homocysteine among mothers were noted as risk factors for CHD (
P |
| doi_str_mv | 10.1038/ejcn.2017.135 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1936269815</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A689286685</galeid><sourcerecordid>A689286685</sourcerecordid><originalsourceid>FETCH-LOGICAL-c660t-481cb075044f0d0e45a7ab6da01274d64b61553357c57e5e0f94feb5045142d63</originalsourceid><addsrcrecordid>eNqNk8Fv0zAUxiMEYmVw5IosISEOS7Hj2E6OY9oAaRIXOFuO89K4cuxiu6DyN_BHz10H61BVTT5Y8vu973Py_BXFa4LnBNPmAyy1m1eYiDmh7EkxI7XgJeM1flrMcMvqkmIsTooXMS4xzkVRPS9OqqYRnFI6K_5ceasSnKGfJqnJOPSRVGdo9JPXm5jAOEDK9Wjl7WbyYTWaOEWUseG2DU2QVOet-W3cAi3AwW1Rj8b2ARz6ZdKItHe5kuUtGkGFhHoTQcWdcBrBBDT5vIf4sng2KBvh1d1-Wny_uvx28bm8_vrpy8X5dak5x6msG6I7LBiu6wH3GGqmhOp4rzCpRN3zuuOEMUqZ0EwAAzy09QBd5hmpq57T0-L9TncV_I81xCQnEzVYqxz4dZSkpbzibUNYRt_-hy79Orh8O1ntXLLkMYq0gtK25Q2_pxbKgjRu8CkovbWW57xpq4bzhh2lGBGMZ0OcqfIAtZ1AUNY7GEw-fqD6GH5ff36Az6uHyeiDBo9q2Hd4t9eQX4ZNY_R2nYx38aHyUfDAP9HBxxhgkKtgJhU2kmC5DYvchkVuwyJzWDL_5m5q626C_h_9Nx333xRzKT_isDfWg4o35WYZTA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1973399686</pqid></control><display><type>article</type><title>Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Elizabeth, K E ; Praveen, S L ; Preethi, N R ; Jissa, V T ; Pillai, M R</creator><creatorcontrib>Elizabeth, K E ; Praveen, S L ; Preethi, N R ; Jissa, V T ; Pillai, M R</creatorcontrib><description>Background/Objectives:
The objective of the study was to assess the role of variations in serum folate, vitamin B12, homocysteine and the presence of genetic polymorphisms as risk factors for congenital heart disease (CHD) in children.
Subjects/Methods:
A total of 32 children with CHD, and their mothers and 32 normal children and their mothers formed the study and control groups, respectively. Serum folate, vitamin B12 and homocysteine as well as genetic polymorphisms MTHFR C677→T, MTHFR A1298→C, MTR A2756→G and MTRR A66→G were assessed.
Results:
Low serum folate and genetic polymorphisms MTHFR C677→T and MTRR A66→G among children and their mothers and high homocysteine among mothers were noted as risk factors for CHD (
P
<0.05). Vitamin B12 levels were normal and showed no association. Presence of MTHFR C677→T and MTRR A66→G, both concurrently among children as well as mothers and simultaneously among mother–child pairs, showed several fold increase in the risk for CHD. On multivariate analysis, the risk factors noted for CHD were presence of MTHFR C677→T among children and their mothers and MTRR A66→G among mothers. Analyses for nutrient–gene interaction revealed significant associations between low serum folate and high serum homocysteine levels, and the presence of selected genetic polymorphisms.
Conclusions:
Low serum folate, high homocysteine and presence of selected genetic polymorphisms among children and their mothers were noted as risk factors for CHD. Nutrient–gene interaction being a modifiable risk factor, the study recommends the use of peri-conceptional folate supplementation with vitamin B12 sufficiency for primary prevention of CHD.</description><identifier>ISSN: 0954-3007</identifier><identifier>EISSN: 1476-5640</identifier><identifier>DOI: 10.1038/ejcn.2017.135</identifier><identifier>PMID: 28876333</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45 ; 45/77 ; 631/61/212 ; 692/308/2056 ; Adult ; Analysis ; Cardiovascular disease ; Cardiovascular diseases ; Case-Control Studies ; Child ; Child, Preschool ; Children ; Clinical Nutrition ; Complications and side effects ; Congenital diseases ; Congenital heart defects ; Congenital heart disease ; Coronary artery disease ; Cyanocobalamin ; Diet therapy ; Dietary supplements ; Distribution ; Epidemiology ; Ferredoxin-NADP Reductase - genetics ; Folic acid ; Folic Acid - blood ; Gene polymorphism ; Gene-Environment Interaction ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Health aspects ; Health risk assessment ; Heart Defects, Congenital - blood ; Heart Defects, Congenital - genetics ; Heart diseases ; Homocysteine ; Homocysteine - blood ; Humans ; Infant ; Internal Medicine ; Measurement ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Methylenetetrahydrofolate reductase ; Methylenetetrahydrofolate Reductase (NADPH2) - genetics ; Mothers ; Multivariate analysis ; Nutrients ; original-article ; Pediatric research ; Physiological aspects ; Polymorphism ; Polymorphism, Single Nucleotide ; Prenatal influences ; Public Health ; Risk analysis ; Risk Factors ; Socioeconomic Factors ; Supplements ; Vitamin B ; Vitamin B 12 - blood ; Vitamin B12 ; Vitamin B12 deficiency ; Young Adult</subject><ispartof>European journal of clinical nutrition, 2017-12, Vol.71 (12), p.1437-1441</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature. 2017</rights><rights>COPYRIGHT 2017 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2017</rights><rights>Macmillan Publishers Limited, part of Springer Nature. 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c660t-481cb075044f0d0e45a7ab6da01274d64b61553357c57e5e0f94feb5045142d63</citedby><cites>FETCH-LOGICAL-c660t-481cb075044f0d0e45a7ab6da01274d64b61553357c57e5e0f94feb5045142d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28876333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Elizabeth, K E</creatorcontrib><creatorcontrib>Praveen, S L</creatorcontrib><creatorcontrib>Preethi, N R</creatorcontrib><creatorcontrib>Jissa, V T</creatorcontrib><creatorcontrib>Pillai, M R</creatorcontrib><title>Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers</title><title>European journal of clinical nutrition</title><addtitle>Eur J Clin Nutr</addtitle><addtitle>Eur J Clin Nutr</addtitle><description>Background/Objectives:
The objective of the study was to assess the role of variations in serum folate, vitamin B12, homocysteine and the presence of genetic polymorphisms as risk factors for congenital heart disease (CHD) in children.
Subjects/Methods:
A total of 32 children with CHD, and their mothers and 32 normal children and their mothers formed the study and control groups, respectively. Serum folate, vitamin B12 and homocysteine as well as genetic polymorphisms MTHFR C677→T, MTHFR A1298→C, MTR A2756→G and MTRR A66→G were assessed.
Results:
Low serum folate and genetic polymorphisms MTHFR C677→T and MTRR A66→G among children and their mothers and high homocysteine among mothers were noted as risk factors for CHD (
P
<0.05). Vitamin B12 levels were normal and showed no association. Presence of MTHFR C677→T and MTRR A66→G, both concurrently among children as well as mothers and simultaneously among mother–child pairs, showed several fold increase in the risk for CHD. On multivariate analysis, the risk factors noted for CHD were presence of MTHFR C677→T among children and their mothers and MTRR A66→G among mothers. Analyses for nutrient–gene interaction revealed significant associations between low serum folate and high serum homocysteine levels, and the presence of selected genetic polymorphisms.
Conclusions:
Low serum folate, high homocysteine and presence of selected genetic polymorphisms among children and their mothers were noted as risk factors for CHD. Nutrient–gene interaction being a modifiable risk factor, the study recommends the use of peri-conceptional folate supplementation with vitamin B12 sufficiency for primary prevention of CHD.</description><subject>45</subject><subject>45/77</subject><subject>631/61/212</subject><subject>692/308/2056</subject><subject>Adult</subject><subject>Analysis</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Children</subject><subject>Clinical Nutrition</subject><subject>Complications and side effects</subject><subject>Congenital diseases</subject><subject>Congenital heart defects</subject><subject>Congenital heart disease</subject><subject>Coronary artery disease</subject><subject>Cyanocobalamin</subject><subject>Diet therapy</subject><subject>Dietary supplements</subject><subject>Distribution</subject><subject>Epidemiology</subject><subject>Ferredoxin-NADP Reductase - genetics</subject><subject>Folic acid</subject><subject>Folic Acid - blood</subject><subject>Gene polymorphism</subject><subject>Gene-Environment Interaction</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Health aspects</subject><subject>Health risk assessment</subject><subject>Heart Defects, Congenital - blood</subject><subject>Heart Defects, Congenital - genetics</subject><subject>Heart diseases</subject><subject>Homocysteine</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Infant</subject><subject>Internal Medicine</subject><subject>Measurement</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Methylenetetrahydrofolate reductase</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</subject><subject>Mothers</subject><subject>Multivariate analysis</subject><subject>Nutrients</subject><subject>original-article</subject><subject>Pediatric research</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prenatal influences</subject><subject>Public Health</subject><subject>Risk analysis</subject><subject>Risk Factors</subject><subject>Socioeconomic Factors</subject><subject>Supplements</subject><subject>Vitamin B</subject><subject>Vitamin B 12 - blood</subject><subject>Vitamin B12</subject><subject>Vitamin B12 deficiency</subject><subject>Young Adult</subject><issn>0954-3007</issn><issn>1476-5640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNk8Fv0zAUxiMEYmVw5IosISEOS7Hj2E6OY9oAaRIXOFuO89K4cuxiu6DyN_BHz10H61BVTT5Y8vu973Py_BXFa4LnBNPmAyy1m1eYiDmh7EkxI7XgJeM1flrMcMvqkmIsTooXMS4xzkVRPS9OqqYRnFI6K_5ceasSnKGfJqnJOPSRVGdo9JPXm5jAOEDK9Wjl7WbyYTWaOEWUseG2DU2QVOet-W3cAi3AwW1Rj8b2ARz6ZdKItHe5kuUtGkGFhHoTQcWdcBrBBDT5vIf4sng2KBvh1d1-Wny_uvx28bm8_vrpy8X5dak5x6msG6I7LBiu6wH3GGqmhOp4rzCpRN3zuuOEMUqZ0EwAAzy09QBd5hmpq57T0-L9TncV_I81xCQnEzVYqxz4dZSkpbzibUNYRt_-hy79Orh8O1ntXLLkMYq0gtK25Q2_pxbKgjRu8CkovbWW57xpq4bzhh2lGBGMZ0OcqfIAtZ1AUNY7GEw-fqD6GH5ff36Az6uHyeiDBo9q2Hd4t9eQX4ZNY_R2nYx38aHyUfDAP9HBxxhgkKtgJhU2kmC5DYvchkVuwyJzWDL_5m5q626C_h_9Nx333xRzKT_isDfWg4o35WYZTA</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Elizabeth, K E</creator><creator>Praveen, S L</creator><creator>Preethi, N R</creator><creator>Jissa, V T</creator><creator>Pillai, M R</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20171201</creationdate><title>Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers</title><author>Elizabeth, K E ; Praveen, S L ; Preethi, N R ; Jissa, V T ; Pillai, M R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c660t-481cb075044f0d0e45a7ab6da01274d64b61553357c57e5e0f94feb5045142d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>45</topic><topic>45/77</topic><topic>631/61/212</topic><topic>692/308/2056</topic><topic>Adult</topic><topic>Analysis</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Children</topic><topic>Clinical Nutrition</topic><topic>Complications and side effects</topic><topic>Congenital diseases</topic><topic>Congenital heart defects</topic><topic>Congenital heart disease</topic><topic>Coronary artery disease</topic><topic>Cyanocobalamin</topic><topic>Diet therapy</topic><topic>Dietary supplements</topic><topic>Distribution</topic><topic>Epidemiology</topic><topic>Ferredoxin-NADP Reductase - genetics</topic><topic>Folic acid</topic><topic>Folic Acid - blood</topic><topic>Gene polymorphism</topic><topic>Gene-Environment Interaction</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genetic Predisposition to Disease</topic><topic>Health aspects</topic><topic>Health risk assessment</topic><topic>Heart Defects, Congenital - blood</topic><topic>Heart Defects, Congenital - genetics</topic><topic>Heart diseases</topic><topic>Homocysteine</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Infant</topic><topic>Internal Medicine</topic><topic>Measurement</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Methylenetetrahydrofolate reductase</topic><topic>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</topic><topic>Mothers</topic><topic>Multivariate analysis</topic><topic>Nutrients</topic><topic>original-article</topic><topic>Pediatric research</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prenatal influences</topic><topic>Public Health</topic><topic>Risk analysis</topic><topic>Risk Factors</topic><topic>Socioeconomic Factors</topic><topic>Supplements</topic><topic>Vitamin B</topic><topic>Vitamin B 12 - blood</topic><topic>Vitamin B12</topic><topic>Vitamin B12 deficiency</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elizabeth, K E</creatorcontrib><creatorcontrib>Praveen, S L</creatorcontrib><creatorcontrib>Preethi, N R</creatorcontrib><creatorcontrib>Jissa, V T</creatorcontrib><creatorcontrib>Pillai, M R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Elizabeth, K E</au><au>Praveen, S L</au><au>Preethi, N R</au><au>Jissa, V T</au><au>Pillai, M R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers</atitle><jtitle>European journal of clinical nutrition</jtitle><stitle>Eur J Clin Nutr</stitle><addtitle>Eur J Clin Nutr</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>71</volume><issue>12</issue><spage>1437</spage><epage>1441</epage><pages>1437-1441</pages><issn>0954-3007</issn><eissn>1476-5640</eissn><abstract>Background/Objectives:
The objective of the study was to assess the role of variations in serum folate, vitamin B12, homocysteine and the presence of genetic polymorphisms as risk factors for congenital heart disease (CHD) in children.
Subjects/Methods:
A total of 32 children with CHD, and their mothers and 32 normal children and their mothers formed the study and control groups, respectively. Serum folate, vitamin B12 and homocysteine as well as genetic polymorphisms MTHFR C677→T, MTHFR A1298→C, MTR A2756→G and MTRR A66→G were assessed.
Results:
Low serum folate and genetic polymorphisms MTHFR C677→T and MTRR A66→G among children and their mothers and high homocysteine among mothers were noted as risk factors for CHD (
P
<0.05). Vitamin B12 levels were normal and showed no association. Presence of MTHFR C677→T and MTRR A66→G, both concurrently among children as well as mothers and simultaneously among mother–child pairs, showed several fold increase in the risk for CHD. On multivariate analysis, the risk factors noted for CHD were presence of MTHFR C677→T among children and their mothers and MTRR A66→G among mothers. Analyses for nutrient–gene interaction revealed significant associations between low serum folate and high serum homocysteine levels, and the presence of selected genetic polymorphisms.
Conclusions:
Low serum folate, high homocysteine and presence of selected genetic polymorphisms among children and their mothers were noted as risk factors for CHD. Nutrient–gene interaction being a modifiable risk factor, the study recommends the use of peri-conceptional folate supplementation with vitamin B12 sufficiency for primary prevention of CHD.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28876333</pmid><doi>10.1038/ejcn.2017.135</doi><tpages>5</tpages></addata></record> |
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| ispartof | European journal of clinical nutrition, 2017-12, Vol.71 (12), p.1437-1441 |
| issn | 0954-3007 1476-5640 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1936269815 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | 45 45/77 631/61/212 692/308/2056 Adult Analysis Cardiovascular disease Cardiovascular diseases Case-Control Studies Child Child, Preschool Children Clinical Nutrition Complications and side effects Congenital diseases Congenital heart defects Congenital heart disease Coronary artery disease Cyanocobalamin Diet therapy Dietary supplements Distribution Epidemiology Ferredoxin-NADP Reductase - genetics Folic acid Folic Acid - blood Gene polymorphism Gene-Environment Interaction Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Health aspects Health risk assessment Heart Defects, Congenital - blood Heart Defects, Congenital - genetics Heart diseases Homocysteine Homocysteine - blood Humans Infant Internal Medicine Measurement Medicine Medicine & Public Health Metabolic Diseases Methylenetetrahydrofolate reductase Methylenetetrahydrofolate Reductase (NADPH2) - genetics Mothers Multivariate analysis Nutrients original-article Pediatric research Physiological aspects Polymorphism Polymorphism, Single Nucleotide Prenatal influences Public Health Risk analysis Risk Factors Socioeconomic Factors Supplements Vitamin B Vitamin B 12 - blood Vitamin B12 Vitamin B12 deficiency Young Adult |
| title | Folate, vitamin B12, homocysteine and polymorphisms in folate metabolizing genes in children with congenital heart disease and their mothers |
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