Maternal Intake of Fat, Riboflavin and Nicotinamide and the Risk of Having Offspring with Congenital Heart Defects

Overview

Journal Eur J Nutr

Specialty Nutritional Sciences

Date 2008 Sep 10

PMID 18779918

Citations 23

Authors

Huberdina P M Smedts

Maryam Rakhshandehroo

Anna C Verkleij-Hagoort

Jeanne H M de Vries

Jaap Ottenkamp

Eric A P Steegers

Regine P M Steegers-Theunissen

Affiliations

Soon will be listed here.

Abstract

Background: With the exception of studies on folic acid, little evidence is available concerning other nutrients in the pathogenesis of congenital heart defects (CHDs). Fatty acids play a central role in embryonic development, and the B-vitamins riboflavin and nicotinamide are co-enzymes in lipid metabolism.

Aim Of The Study: To investigate associations between the maternal dietary intake of fats, riboflavin and nicotinamide, and CHD risk in the offspring.

Methods: A case-control family study was conducted in 276 mothers of a child with a CHD comprising of 190 outflow tract defects (OTD) and 86 non-outflow tract defects (non-OTD) and 324 control mothers of a non-malformed child. Mothers filled out general and food frequency questionnaires at 16 months after the index-pregnancy, as a proxy of the habitual food intake in the preconception period. Nutrient intakes (medians) were compared between cases and controls by Mann-Whitney U test. Odds ratios (OR) for the association between CHDs and nutrient intakes were estimated in a logistic regression model.

Results: Case mothers, in particular mothers of a child with OTD, had higher dietary intakes of saturated fat, 30.9 vs. 29.8 g/d; P < 0.05. Dietary intakes of riboflavin and nicotinamide were lower in mothers of a child with an OTD than in controls (1.32 vs. 1.41 mg/d; P < 0.05 and 14.6 vs. 15.1 mg/d; P < 0.05, respectively). Energy, unsaturated fat, cholesterol and folate intakes were comparable between the groups. Low dietary intakes of both riboflavin (<1.20 mg/d) and nicotinamide (<13.5 mg/d) increased more than two-fold the risk of a child with an OTD, especially in mothers who did not use vitamin supplements in the periconceptional period (OR 2.4, 95%CI 1.4-4.0). Increasing intakes of nicotinamide (OR 0.8, 95%CI 0.7-1.001, per unit standard deviation increase) decreased CHD risk independent of dietary folate intake.

Conclusions: A maternal diet high in saturated fats and low in riboflavin and nicotinamide seems to contribute to CHD risk, in particular OTDs.

Citing Articles

The Effect of Maternal Exposure to a Diet High in Fats and Cholesterol on the Placental Function and Phenotype of the Offspring in a Rabbit Model: A Summary Review of About 15 Years of Research.

Rousseau-Ralliard D, Chavatte-Palmer P, Couturier-Tarrade A Int J Mol Sci. 2023; 24(19).

PMID: 37834002 PMC: 10572169. DOI: 10.3390/ijms241914547.

An Evaluation of Food and Nutrient Intake among Pregnant Women in The Netherlands: A Systematic Review.

Ter Borg S, Koopman N, Verkaik-Kloosterman J Nutrients. 2023; 15(13).

PMID: 37447397 PMC: 10346763. DOI: 10.3390/nu15133071.

Dietary Inflammatory Index during Pregnancy and Congenital Heart Defects.

Yang J, Chang Q, Du Q, Dang S, Zeng L, Yan H Nutrients. 2023; 15(10).

PMID: 37242143 PMC: 10222117. DOI: 10.3390/nu15102262.

Gestational palmitic acid suppresses embryonic GATA-binding protein 4 signaling and causes congenital heart disease.

Zhao R, Cao L, Gu W, Li L, Chen Z, Xiang J Cell Rep Med. 2023; 4(3):100953.

PMID: 36809766 PMC: 10040382. DOI: 10.1016/j.xcrm.2023.100953.

Response to the letter to editor: Can niacin supplementation prevent congenital malformations associated with maternal use of proton pump inhibitors?.

Palawaththa S, Islam R, Ilic D, Rabel K, Lee M, Romeo L Eur J Nutr. 2022; 62(2):1055-1056.

PMID: 36449092 DOI: 10.1007/s00394-022-03061-0.

References

Vujkovic M, Ocke M, van der Spek P, Yazdanpanah N, Steegers E, Steegers-Theunissen R . Maternal Western dietary patterns and the risk of developing a cleft lip with or without a cleft palate. Obstet Gynecol. 2007; 110(2 Pt 1):378-84. DOI: 10.1097/01.AOG.0000268799.37044.c3. View

Gittenberger-de Groot A, Bartelings M, DeRuiter M, Poelmann R . Basics of cardiac development for the understanding of congenital heart malformations. Pediatr Res. 2004; 57(2):169-76. DOI: 10.1203/01.PDR.0000148710.69159.61. View

Shaw G, Carmichael S, Laurent C, Rasmussen S . Maternal nutrient intakes and risk of orofacial clefts. Epidemiology. 2006; 17(3):285-91. DOI: 10.1097/01.ede.0000208348.30012.35. View

de Walle H, de Jong-van den Berg L . Growing gap in folic acid intake with respect to level of education in the Netherlands. Community Genet. 2007; 10(2):93-6. DOI: 10.1159/000099086. View

Feunekes G, van Staveren W, de Vries J, BUREMA J, Hautvast J . Relative and biomarker-based validity of a food-frequency questionnaire estimating intake of fats and cholesterol. Am J Clin Nutr. 1993; 58(4):489-96. DOI: 10.1093/ajcn/58.4.489. View

Hoffman J, Kaplan S . The incidence of congenital heart disease. J Am Coll Cardiol. 2002; 39(12):1890-900. DOI: 10.1016/s0735-1097(02)01886-7. View

Boot M, Steegers-Theunissen R, Poelmann R, Van Iperen L, Lindemans J, Gittenberger-de Groot A . Folic acid and homocysteine affect neural crest and neuroepithelial cell outgrowth and differentiation in vitro. Dev Dyn. 2003; 227(2):301-8. DOI: 10.1002/dvdy.10303. View

Willett W, Howe G, Kushi L . Adjustment for total energy intake in epidemiologic studies. Am J Clin Nutr. 1997; 65(4 Suppl):1220S-1228S; discussion 1229S-1231S. DOI: 10.1093/ajcn/65.4.1220S. View

Waterland R, Michels K . Epigenetic epidemiology of the developmental origins hypothesis. Annu Rev Nutr. 2007; 27:363-88. DOI: 10.1146/annurev.nutr.27.061406.093705. View

10.

Khan I, Dekou V, Douglas G, Jensen R, Hanson M, Poston L . A high-fat diet during rat pregnancy or suckling induces cardiovascular dysfunction in adult offspring. Am J Physiol Regul Integr Comp Physiol. 2004; 288(1):R127-33. DOI: 10.1152/ajpregu.00354.2004. View

11.

Botto L, Mulinare J, Erickson J . Do multivitamin or folic acid supplements reduce the risk for congenital heart defects? Evidence and gaps. Am J Med Genet A. 2003; 121A(2):95-101. DOI: 10.1002/ajmg.a.20132. View

12.

Verkleij-Hagoort A, de Vries J, Stegers M, Lindemans J, Ursem N, Steegers-Theunissen R . Validation of the assessment of folate and vitamin B12 intake in women of reproductive age: the method of triads. Eur J Clin Nutr. 2006; 61(5):610-5. DOI: 10.1038/sj.ejcn.1602581. View

13.

Groenen P, van Rooij I, Peer P, Ocke M, Zielhuis G, Steegers-Theunissen R . Low maternal dietary intakes of iron, magnesium, and niacin are associated with spina bifida in the offspring. J Nutr. 2004; 134(6):1516-22. DOI: 10.1093/jn/134.6.1516. View

14.

Goldberg G, Black A, Jebb S, Cole T, Murgatroyd P, Coward W . Critical evaluation of energy intake data using fundamental principles of energy physiology: 1. Derivation of cut-off limits to identify under-recording. Eur J Clin Nutr. 1991; 45(12):569-81. View

15.

Krapels I, van Rooij I, Ocke M, Van Cleef B, Kuijpers-Jagtman A, Steegers-Theunissen R . Maternal dietary B vitamin intake, other than folate, and the association with orofacial cleft in the offspring. Eur J Nutr. 2004; 43(1):7-14. DOI: 10.1007/s00394-004-0433-y. View

16.

Watkins M, Rasmussen S, Honein M, Botto L, Moore C . Maternal obesity and risk for birth defects. Pediatrics. 2003; 111(5 Pt 2):1152-8. View

17.

Nielsen G, Norgard B, Puho E, Rothman K, Sorensen H, Czeizel A . Risk of specific congenital abnormalities in offspring of women with diabetes. Diabet Med. 2005; 22(6):693-6. DOI: 10.1111/j.1464-5491.2005.01477.x. View

18.

Powers H . Riboflavin (vitamin B-2) and health. Am J Clin Nutr. 2003; 77(6):1352-60. DOI: 10.1093/ajcn/77.6.1352. View

19.

Brauer P, Rosenquist T . Effect of elevated homocysteine on cardiac neural crest migration in vitro. Dev Dyn. 2002; 224(2):222-30. DOI: 10.1002/dvdy.10105. View

20.

Hobbs C, Malik S, Zhao W, James S, Melnyk S, Cleves M . Maternal homocysteine and congenital heart defects. J Am Coll Cardiol. 2006; 47(3):683-5. DOI: 10.1016/j.jacc.2005.11.013. View