Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children

Carina Venter; Michaela P. Palumbo; Katherine A. Sauder; Deborah H. Glueck; Liam O’Mahony; Ivana Yang; Elizabeth J. Davidson; Helen A. Brough; John W. Holloway; David M. Fleischer; Miriam Ben-Abdallah; Dana Dabelea

doi:10.1111/pai.13753

Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children

Carina Venter^*, Michaela P. Palumbo, Katherine A. Sauder, Deborah H. Glueck, Liam O’Mahony, Ivana Yang, Elizabeth J. Davidson, Helen A. Brough, John W. Holloway, David M. Fleischer, Miriam Ben-Abdallah, Dana Dabelea

^*Corresponding author for this work

Women & Children's Health

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

Background: Filaggrin (FLG) loss-of-function mutations in children and maternal diet in pregnancy have been implicated in child allergy outcomes. This paper studies the questions: “do FLG mutations modify the effect of maternal diet on the odds of development of allergic diseases?” and “which factor leads to the highest rate of diagnosis allergic diseases over time, maternal diet, or FLG mutations?”. Methods: Exact logistic regressions studied effect modification. Cox proportional hazard models compared the rate of allergic disease development in three groups (N = 624): (1) children with FLG mutation, (2) children without FLG mutation whose mothers did not eat an allergy preventive diet, and (3) children without FLG mutation whose mothers ate an allergy preventive diet. Maternal diet was classified using a validated index. Results: Cox models showed the development of atopic dermatitis, asthma, and wheeze was significantly higher for children in group 1 versus 3 (HR = 2.40 [1.32, 4.37], HR = 2.29 [1.05, 4.97], and HR 2.10 [1.004, 4.38], respectively), but not significantly higher for children in group 1 versus 2 (HR = 1.30 [0.74, 2.29], HR = 1.27 [0.61, 2.63], and HR = 1.29 [0.65, 2.58], respectively). Development of allergic rhinitis was significantly higher for group 1 versus 2 and 3 (1 vs. 2: HR = 2.29 [1.10, 4.76]; 1 vs. 3: HR = 3.21 [1.46, 7.08]). There was no significant effect modification for any outcome. Conclusion: Children with FLG mutation had similar risk of atopic dermatitis, asthma, and wheeze as children without an FLG mutation whose mothers did not eat an allergy preventive diet during pregnancy. Child FLG mutation did not modify the effect of maternal diet. The results suggest that maternal diet in pregnancy, a modifiable risk factor, could be a target for preventive interventions.

Original language	English
Article number	e13753
Journal	Pediatric Allergy and Immunology
Volume	33
Issue number	3
DOIs	https://doi.org/10.1111/pai.13753
Publication status	Published - Mar 2022

Keywords

allergic rhinitis
allergy
asthma
atopic dermatitis
filaggrin
FLG mutation
maternal diet
pregnancy
prevention

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10.1111/pai.13753

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Venter, C., Palumbo, M. P., Sauder, K. A., Glueck, D. H., O’Mahony, L., Yang, I., Davidson, E. J., Brough, H. A., Holloway, J. W., Fleischer, D. M., Ben-Abdallah, M., & Dabelea, D. (2022). Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children. Pediatric Allergy and Immunology, 33(3), Article e13753. https://doi.org/10.1111/pai.13753

@article{94745b88541b423ab2ebbc705c38c4b6,

title = "Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children",

abstract = "Background: Filaggrin (FLG) loss-of-function mutations in children and maternal diet in pregnancy have been implicated in child allergy outcomes. This paper studies the questions: “do FLG mutations modify the effect of maternal diet on the odds of development of allergic diseases?” and “which factor leads to the highest rate of diagnosis allergic diseases over time, maternal diet, or FLG mutations?”. Methods: Exact logistic regressions studied effect modification. Cox proportional hazard models compared the rate of allergic disease development in three groups (N = 624): (1) children with FLG mutation, (2) children without FLG mutation whose mothers did not eat an allergy preventive diet, and (3) children without FLG mutation whose mothers ate an allergy preventive diet. Maternal diet was classified using a validated index. Results: Cox models showed the development of atopic dermatitis, asthma, and wheeze was significantly higher for children in group 1 versus 3 (HR = 2.40 [1.32, 4.37], HR = 2.29 [1.05, 4.97], and HR 2.10 [1.004, 4.38], respectively), but not significantly higher for children in group 1 versus 2 (HR = 1.30 [0.74, 2.29], HR = 1.27 [0.61, 2.63], and HR = 1.29 [0.65, 2.58], respectively). Development of allergic rhinitis was significantly higher for group 1 versus 2 and 3 (1 vs. 2: HR = 2.29 [1.10, 4.76]; 1 vs. 3: HR = 3.21 [1.46, 7.08]). There was no significant effect modification for any outcome. Conclusion: Children with FLG mutation had similar risk of atopic dermatitis, asthma, and wheeze as children without an FLG mutation whose mothers did not eat an allergy preventive diet during pregnancy. Child FLG mutation did not modify the effect of maternal diet. The results suggest that maternal diet in pregnancy, a modifiable risk factor, could be a target for preventive interventions.",

keywords = "allergic rhinitis, allergy, asthma, atopic dermatitis, filaggrin, FLG mutation, maternal diet, pregnancy, prevention",

author = "Carina Venter and Palumbo, {Michaela P.} and Sauder, {Katherine A.} and Glueck, {Deborah H.} and Liam O{\textquoteright}Mahony and Ivana Yang and Davidson, {Elizabeth J.} and Brough, {Helen A.} and Holloway, {John W.} and Fleischer, {David M.} and Miriam Ben-Abdallah and Dana Dabelea",

note = "Funding Information: This work was supported by the National Institutes of Health (NIH), grant numbers: R01 DK076648/DK/NIDDK NIH HHS/United States, R01 GM121081/GM/NIGMS NIH HHS/United States, UG3 OD023248/OD/NIH HHS/United States, UH3 OD023248/OD/NIH HHS/United States, R25GM111901-S1, R25GM11190, NIH grant R00ES025817. This work was supported by the National Institutes of Health (NIH), grant numbers: R01 DK076648/DK/NIDDK NIH HHS/United States, R01 GM121081/GM/NIGMS NIH HHS/United States, UG3 OD023248/OD/NIH HHS/United States, UH3 OD023248/OD/NIH HHS/United States, R25GM111901-S1, R25GM11190, NIH grant R00ES025817. Funding Information: This work was supported by University of Buenos Aires (UBACyT 20020130100610BA for MJ & 2002017010755BA for BCB), Agencia Nacional de Promoci{\'o}n Cient{\'i}fica y Tecnol{\'o}gica (ANPCyT PICT 2012-1167 for MJ), Fundaci{\'o}n Argentina de Nanotecnolog{\'i}a (Proyecto Presemillas for BCB) and National Research Council of Argentina (CONICET PIP 11220170100991CO for MJ). Authors thanks Dr. Claudia Marchi for her remarkable help in the FESEM images. VO is a member of ALN. Publisher Copyright: {\textcopyright} 2022 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.",

year = "2022",

month = mar,

doi = "10.1111/pai.13753",

language = "English",

volume = "33",

journal = "Pediatric Allergy and Immunology",

issn = "0905-6157",

publisher = "Blackwell Munksgaard",

number = "3",

}

Venter, C, Palumbo, MP, Sauder, KA, Glueck, DH, O’Mahony, L, Yang, I, Davidson, EJ, Brough, HA, Holloway, JW, Fleischer, DM, Ben-Abdallah, M & Dabelea, D 2022, 'Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children', Pediatric Allergy and Immunology, vol. 33, no. 3, e13753. https://doi.org/10.1111/pai.13753

TY - JOUR

T1 - Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children

AU - Venter, Carina

AU - Palumbo, Michaela P.

AU - Sauder, Katherine A.

AU - Glueck, Deborah H.

AU - O’Mahony, Liam

AU - Yang, Ivana

AU - Davidson, Elizabeth J.

AU - Brough, Helen A.

AU - Holloway, John W.

AU - Fleischer, David M.

AU - Ben-Abdallah, Miriam

AU - Dabelea, Dana

N1 - Funding Information: This work was supported by the National Institutes of Health (NIH), grant numbers: R01 DK076648/DK/NIDDK NIH HHS/United States, R01 GM121081/GM/NIGMS NIH HHS/United States, UG3 OD023248/OD/NIH HHS/United States, UH3 OD023248/OD/NIH HHS/United States, R25GM111901-S1, R25GM11190, NIH grant R00ES025817. This work was supported by the National Institutes of Health (NIH), grant numbers: R01 DK076648/DK/NIDDK NIH HHS/United States, R01 GM121081/GM/NIGMS NIH HHS/United States, UG3 OD023248/OD/NIH HHS/United States, UH3 OD023248/OD/NIH HHS/United States, R25GM111901-S1, R25GM11190, NIH grant R00ES025817. Funding Information: This work was supported by University of Buenos Aires (UBACyT 20020130100610BA for MJ & 2002017010755BA for BCB), Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT PICT 2012-1167 for MJ), Fundación Argentina de Nanotecnología (Proyecto Presemillas for BCB) and National Research Council of Argentina (CONICET PIP 11220170100991CO for MJ). Authors thanks Dr. Claudia Marchi for her remarkable help in the FESEM images. VO is a member of ALN. Publisher Copyright: © 2022 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.

PY - 2022/3

Y1 - 2022/3

N2 - Background: Filaggrin (FLG) loss-of-function mutations in children and maternal diet in pregnancy have been implicated in child allergy outcomes. This paper studies the questions: “do FLG mutations modify the effect of maternal diet on the odds of development of allergic diseases?” and “which factor leads to the highest rate of diagnosis allergic diseases over time, maternal diet, or FLG mutations?”. Methods: Exact logistic regressions studied effect modification. Cox proportional hazard models compared the rate of allergic disease development in three groups (N = 624): (1) children with FLG mutation, (2) children without FLG mutation whose mothers did not eat an allergy preventive diet, and (3) children without FLG mutation whose mothers ate an allergy preventive diet. Maternal diet was classified using a validated index. Results: Cox models showed the development of atopic dermatitis, asthma, and wheeze was significantly higher for children in group 1 versus 3 (HR = 2.40 [1.32, 4.37], HR = 2.29 [1.05, 4.97], and HR 2.10 [1.004, 4.38], respectively), but not significantly higher for children in group 1 versus 2 (HR = 1.30 [0.74, 2.29], HR = 1.27 [0.61, 2.63], and HR = 1.29 [0.65, 2.58], respectively). Development of allergic rhinitis was significantly higher for group 1 versus 2 and 3 (1 vs. 2: HR = 2.29 [1.10, 4.76]; 1 vs. 3: HR = 3.21 [1.46, 7.08]). There was no significant effect modification for any outcome. Conclusion: Children with FLG mutation had similar risk of atopic dermatitis, asthma, and wheeze as children without an FLG mutation whose mothers did not eat an allergy preventive diet during pregnancy. Child FLG mutation did not modify the effect of maternal diet. The results suggest that maternal diet in pregnancy, a modifiable risk factor, could be a target for preventive interventions.

AB - Background: Filaggrin (FLG) loss-of-function mutations in children and maternal diet in pregnancy have been implicated in child allergy outcomes. This paper studies the questions: “do FLG mutations modify the effect of maternal diet on the odds of development of allergic diseases?” and “which factor leads to the highest rate of diagnosis allergic diseases over time, maternal diet, or FLG mutations?”. Methods: Exact logistic regressions studied effect modification. Cox proportional hazard models compared the rate of allergic disease development in three groups (N = 624): (1) children with FLG mutation, (2) children without FLG mutation whose mothers did not eat an allergy preventive diet, and (3) children without FLG mutation whose mothers ate an allergy preventive diet. Maternal diet was classified using a validated index. Results: Cox models showed the development of atopic dermatitis, asthma, and wheeze was significantly higher for children in group 1 versus 3 (HR = 2.40 [1.32, 4.37], HR = 2.29 [1.05, 4.97], and HR 2.10 [1.004, 4.38], respectively), but not significantly higher for children in group 1 versus 2 (HR = 1.30 [0.74, 2.29], HR = 1.27 [0.61, 2.63], and HR = 1.29 [0.65, 2.58], respectively). Development of allergic rhinitis was significantly higher for group 1 versus 2 and 3 (1 vs. 2: HR = 2.29 [1.10, 4.76]; 1 vs. 3: HR = 3.21 [1.46, 7.08]). There was no significant effect modification for any outcome. Conclusion: Children with FLG mutation had similar risk of atopic dermatitis, asthma, and wheeze as children without an FLG mutation whose mothers did not eat an allergy preventive diet during pregnancy. Child FLG mutation did not modify the effect of maternal diet. The results suggest that maternal diet in pregnancy, a modifiable risk factor, could be a target for preventive interventions.

KW - allergic rhinitis

KW - allergy

KW - asthma

KW - atopic dermatitis

KW - filaggrin

KW - FLG mutation

KW - maternal diet

KW - pregnancy

KW - prevention

UR - http://www.scopus.com/inward/record.url?scp=85127295683&partnerID=8YFLogxK

U2 - 10.1111/pai.13753

DO - 10.1111/pai.13753

M3 - Article

C2 - 35338739

AN - SCOPUS:85127295683

SN - 0905-6157

VL - 33

JO - Pediatric Allergy and Immunology

JF - Pediatric Allergy and Immunology

IS - 3

M1 - e13753

ER -

Associations between child filaggrin mutations and maternal diet with the development of allergic diseases in children

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