# paper.pdf ## Metadata - PDFFormatVersion=1.7 - Language=en-US - IsLinearized=true - IsAcroFormPresent=false - IsXFAPresent=false - IsCollectionPresent=false - IsSignaturesPresent=false - CreationDate=D:20260506185622+05'30' - Creator=Adobe InDesign 19.5 (Windows) - ModDate=D:20260506185625+05'30' - Producer=Adobe PDF Library 17.0 - Title=Excessive gestational weight gain and risk of asthma, rhinitis and allergic sensitization: Results from a Portuguese birth cohort - Trapped=False - Custom.WPS-ARTICLEDOI=10.1111/pai.70357 - Custom.WPS-JOURNALDOI=10.1111/(ISSN)1399-3038 - Custom.WPS-PROCLEVEL=3 - jav:journal_article_version=VoR - prism:doi=10.1111/pai.70357 - pdfx:wps-articledoi=10.1111/pai.70357 - pdfx:wps-journaldoi=10.1111/(ISSN)1399-3038 - pdfx:wps-proclevel=3 - dc:title=Excessive gestational weight gain and risk of asthma, rhinitis and allergic sensitization: Results from a Portuguese birth cohort ## Contents ### Page 1 Pediatr Allergy Immunol. 2026;37:e70357. | 1 of 13https://doi.org/10.1111/pai.70357wileyonlinelibrary.com/journal/paiReceived: 6 August 2025 | Revised: 8 April 2026 | Accepted: 15 April 2026DOI: 10.1111/pai.70357O R I G I N A L A R T I C L E Excessive gestational weight gain and risk of asthma, rhinitis and allergic sensitization: Results from a Portuguese birth cohort Mónica Rodrigues1,2 | Susana Santos1 | Francisca Castro Mendes1,3 |Pedro Moreira1,4 | André Moreira1,2,3,4,51 EPIUnit ITR, Institute of Public Health of the University Porto, University of Porto, Porto, Portugal 2 Public Health and Forensic Sciences and Medical Education Department, Faculty of Medicine, University of Porto, Porto, Portugal 3 Basic and Clinical Immunology, Department of Pathology, Faculty of Medicine, University of Porto, Porto, Portugal 4 Faculty of Nutrition and Food Sciences, University of Porto, Porto, Portugal 5 Immuno-Allergology Department, Centro Hospitalar São João, Porto, PortugalCorrespondenceMónica Rodrigues, EPIUnit ITR, Institute of Public Health of the University Porto, University of Porto, Rua das Taipas, n° 135, Porto 4050-600, Portugal. Email: monicarodrigues@med.up.ptFunding informationFundação para a Ciência e a Tecnologia, Grant/Award Number: 2023.02362.BD, UIDB/04750/2020 and LA/P/0064/2020; Marie Curie, Grant/Award Number: 101109136Editor: Jon GenuneitAbstract Background: Maternal body mass index (BMI) before pregnancy and gestational weight gain (GWG) have been implicated in offspring health, yet their specific impact on the development of allergic diseases remains unclear. We aimed to evaluate associations between pre- pregnancy BMI and GWG with asthma, rhinitis, eczema, food allergy, anaphylaxis, and allergic sensitization during childhood and adolescence.Methods: We analyzed 7280 mother–child pairs from Generation XXI, a Portuguesepopulation-based birth cohort. Maternal BMI was categorized per World Health Organization criteria and grouped into underweight/normal weight vs. overweight/ obesity. GWG was considered using Institute of Medicine (IOM) guidelines and GWGz-scores. Allergic outcomes were assessed via parent-reported physician diagnosisat 4, 7, 10, and 13 years, and allergic sensitization was determined at 10 years usingImmunoCAP. Associations were analyzed using logistic regression models adjusted for confounders.Results: Children of mothers with excessive GWG had increased odds of asthmaat ages 7 and 13 (aOR = 1.30; 95% CI 1.01–1.66 and aOR = 1.29; 95% CI 1.01–1.65,respectively), and rhinitis at 4 (OR = 1.48; 95% CI 1.10–1.98). Higher GWG z-scoregroup was associated with increased odds of asthma (aOR = 1.33; 95% CI 1.03–1.72),rhinitis (aOR = 1.54; 95% CI 1.13–2.09), and sensitization (aOR = 1.44; 95% CI 1.05–1.97). Lower GWG z-score group was associated to higher eczema odds at 13, while higher reduced eczema odds at age 4. Maternal overweight/obesity was associatedwith lower odds of eczema at age 13 (aOR = 0.73; 95% CI 0.60–0.88). Apart fromeczema, maternal BMI showed no significant associations with others allergic diseases.Conclusion: Higher GWG is associated with increased odds of childhood asthma, rhinitis, and sensitization. In contrast, maternal overweight/obesity is linked to lower odds of eczema, suggesting condition-specific effects of maternal weight on childhood allergy risk. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. © 2026 The Author(s). Pediatric Allergy and Immunology published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd. ### Page 2 2 of 13 |RODRIGUES et al.1 | I NTRO D U C TI O NAllergic diseases are among the most common chronic conditions in childhood and have become a global public health concern. These immune-mediated disorders result from complex interactions between genetic predisposition and environmental exposures. The increasing prevalence of allergic diseases worldwide, documented in both the International Study of Asthma and Allergies in Childhood (ISAAC) and Global Asthma Network studies, highlights the need to understand early-life determinants that could guide preventive strategies.1,2 The prenatal period represents a critical window for immune system programming and growth development, including the lungs. During this time, environmental exposures, as maternal nutritional status, may influence the fetal epigenome and shape immune system and airways development, potentially altering asthma and other allergies risk in later life. Maternal body mass index (BMI) before pregnancy and gestational weight gain (GWG) have been identified as modifiable exposures that may influence offspring health outcomes.3–19 Emerging evidence links higher maternal BMI with increased risk of asthma and wheezing in children,3–15,20–22 while the role of GWG remains less consistent and less studied, especially in relation to allergic diseases beyond asthma.11,14,20,22 Importantly, previous studies have shown methodological heterogeneity in defining GWG, often failing to account for pre-pregnancy BMI or gestational age. The Institute of Medicine (IOM) guidelines offer a BMI-specific framework for GWG recommenda- tions, yet adherence to these guidelines remains suboptimal glob- ally. 23 Additionally, no studies on this theme have utilized GWG reference charts considering maternal BMI and gestational age, which could provide a more individualized assessment of weight gain adequacy. Considering this we aimed to investigate the associations be- tween maternal pre-pregnancy BMI and GWG—classified using both IOM criteria and GWG z-scores—with the development of asthma, rhinitis, eczema, food allergy, anaphylaxis, and allergic sensitization in offspring from early childhood through adolescence.2 | M E TH O DS 2.1 | Study participantsThis study is part of Generation XXI (G21), which is a prospectivepopulation-based birth cohort. 24,25 Between April 2005–August2006, mothers and newborns from all public obstetrical and neonatal care units in the metropolitan area of Porto, Portugal, were invited to participate. At the time of enrollment, these units accounted for92% of all deliveries in the region. A total of 8495 mothers (92%) and 8647 newborns accepted toparticipate. These participants were re-evaluated at the age of 4 (n = 7459, 86%), 7 (n = 6889, 80%), 10 (n = 6397, 74%), and 13 yearsof age (n = 4640, 54%). In this study, we excluded 296 twins, 299 mother–child pairswithout information on weight or height before pregnancy and916 without information on allergic diseases, leaving up 7280 par- ticipants for our analysis regarding the association between BMI pre-pregnancy and allergic diseases. Further, 373 participants were excluded due to not having information on GWG, 4 due to aweight gain below −20 kg and 3 due to a GWG z-score below −14,leaving 6901 mother–child pairs for our analysis regarding the as- sociation between GWG and allergic diseases. For all the models, the sample size varied according to the sample size of the differ- ent variables at different ages. More information on the Flowchart is presented in Figure S1. Regarding differences between included and excluded participants, included participants were more likely to have older and more educated mothers, and a lower prevalence of maternal smoking during pregnancy. Additionally, some allergic out- comes were more frequently reported among included participants. However, key variables were included in the adjusted models and according to Cohen's h and d and Cramér's V, effect size values were not substantial, <0.30. 26,27 A detailed comparison of included and excluded participants is presented in Table S1.2.2 | Ethical considerationsAll phases complied with Ethical Principles for Medical Research Involving Human Subjects in the Declaration of Helsinki*. All evaluations were approved by the University of Porto Medical School/São João Hospital Centre Ethics Committee, except the 13-year follow-up that was approved by the ISPUP Ethics Committee. Procedures were explained to participants, and an informed consent was signed by one of the parents/legal guardians (at13 years also signed by participants). The baseline evaluation wasK E Y W O R D Sallergic diseases, body mass index, early life exposures, gestational weight gain, perinatal healthKey messageExcessive gestational weight gain is a modifiable risk factor associated with an increased risk of asthma, rhinitis, and allergic sensitization in children, underscoring the importance of maintaining a healthy maternal weight during pregnancy. ### Page 3 | 3 of 13RODRIGUES et al.additionally approved by the Data Protection National Commission and the study follows the present EU General Data Protection Regulation under close supervision of the Data Protection Office of ISPUP. *World Medical Association Declaration of Helsinki, 2013. Available at: https://www.wma.net/what-we-do/medic al-ethics/declaration-of-helsinki/.2.3 | Maternal anthropometricsBaseline information was gathered either through direct interviewsor from medical records. Within 72 h after childbirth, trainedinterviewers conducted face-to-face interviews and evaluations using structured questionnaires and standardized procedures. Pre-pregnancy weight was used as the baseline measure to es- timate pre-pregnancy BMI and GWG. Pre-pregnancy weight was based on a self-report and defined as the usual body weight before pregnancy, weight at the beginning of pregnancy, or in the first pre-natal medical visit if it occurred before the 13th gestational week. The mother reported the weight at the end of pregnancy at enrollment. Weight was retrieved from clinical records for moth- ers who did not provide this information. The interviewer mea-sured height at recruitment to the nearest 0.1 cm without shoes. Ifmeasurement was not possible, height was taken from the national ID card. Maternal pre-pregnancy BMI was calculated and categorized according to World Health Organization (WHO) definition: under- weight (<18.5 kg/m2), normal weight (18.5–24.9 kg/m2 ), overweight(25.0–29.9 kg/m2) and obesity (≥30.00 kg/m2 ).28 For the association between maternal BMI and allergic diseases, BMI was classified into two categories: underweight/normal weight and overweight/ obesity. Further sensitivity analyses with the four pre-pregnancy maternal BMI categories, excluding the underweight category, are presented in Data S1. GWG was defined as the difference between the weight be- fore delivery and pre-pregnancy weight. Women were categorized as gaining below (insufficient GWG), as recommended (adequate GWG), or above (excessive GWG) the IOM recommendations ac- cording to maternal pre-pregnancy BMI. 29 We also calculated GWGz-scores based on pre-pregnancy BMI group-specific reference charts for gestational weight gain which also considers gestationalage, derived using data from 218,216 pregnant women across 33 co- horts in Europe, North America, and Oceania. 30 GWG z-scores werealso further categorized according to tertiles (1st: ≤ −0.48; 2nd: >−0.48 and ≤0.43; 3rd: >0.43).2.4 | Allergic outcomesData on allergic outcomes were collected through questionnaires based on the ISAAC standardized questionnaire. Asthma (4, 7, 10,13 years), rhinitis (4, 7, 13 years), food allergy (13 years), anaphylaxis(13 years), and eczema (4, 7, 13 years) were defined as a positiveanswer to “Has your child/the adolescent ever been diagnosed with asthma/rhinitis/eczema/food allergy/anaphylaxis by a physician?” For allergic sensitization, among the 6397 children evaluated at 10-year follow-up, blood samples were collected from 4047 partici- pants. From this group, a subset of 1125 children was selected using a computer-generated randomization sequence to assess specific IgE levels through the ImmunoCAP Phadiatop Infant test (Thermo Fisher Scientific, Uppsala, Sweden). A child was considered to have allergic sensitization if the specific IgE level was 0.35 kU/L or higher for at least one of the tested aeroallergens or food allergens. 312.5 | CovariatesCovariates were selected according to previous literature if they were related to pre-pregnancy BMI or GWG and allergic dis- eases. 32,33 Using a direct acyclic graph, DAG, we confirmed that all covariates reach the graphical criteria for confounding, ensuring ap- propriate control and clarifying the assumed relationships among variables. This included: maternal age at birth (in years); sex of the children; maternal education at baseline assessed through the num-ber of completed schooling years and categorized into ≤9, 10–12,or >12 years34 ; parity (primiparous/multiparous); maternal smoking status during pregnancy (ever vs. no smoking); and mother history of allergic diseases which was considered if a positive answer to the question “Before becoming pregnant, has a doctor ever diagnosedyou with an illness – asthma/allergy/rhinitis – that compels you orhas forced you to continue treatment?” was provided. DAG Figures are presented in Figures S2 and S3.2.6 | Statistical analysisContinuous variables are presented as mean values and standard deviation (±SD) as they were normally distributed. Categorical variables are described as counts and proportions. To determine differences between groups, the t-student test for independent variables and the One Way ANOVA tests were used for continuous normally distributed variables, according to the number of groups in the categorical variable. The chi-square test was used for categorical variables. Logistic regression models in crude and adjusted models were used to study the association between pre-pregnancy BMI and GWG with allergic diseases, and the magnitude of the associationwas measured by Odds Ratio (OR) and its respective 95% confidenceintervals (CI). For our adjusted models we used the following covari- ates: sex of the children, maternal age, maternal education, parity, maternal history of allergic diseases and maternal smoking during pregnancy. We further adjusted for maternal pre-pregnancy BMI when studying the association between GWG and GWG z-scores with allergic diseases. Child BMI was considered a potential medi- ator in the pathway between maternal weight status and allergic outcomes. Therefore, it was not included in the regression models ### Page 4 4 of 13 |RODRIGUES et al.to estimate the total effect of maternal nutritional status. Based on prior literature suggesting that the effects of GWG on child health outcomes may differ according to maternal BMI 35 we also explored the association between GWG with allergic diseases considering two categories of maternal pre-pregnancy BMI (underweight/normal weight and overweight/obesity), interaction analysis are presented in Supplementarial material, Table 2. We observed a consistent in- teraction between GWG and sex regarding asthma, accordingly, we performed stratified analysis for this outcome, present on Table S3. Additionally, we fitted Generalized Estimating Equations models for asthma, rhinitis, and eczema to estimate the average effect of ma- ternal factors across ages, while accounting for the correlation be- tween repeated measures within participants. Results are presented in the Tables S4–S8. Multiple regression imputation was performed for covariates with missing data. The maximum proportion of miss-ing values was 4.2% and ten imputed datasets were created. All anal- yses were performed in the IBM SPSS Statistics version 27 and R software version 4.2.1.3 | R E S U LT SThe final analysis comprised 7280 mother–child pairs with data onmaternal pre-pregnancy BMI (Table 1) and 6901 with information on GWG (Table 2). Of these, 31% of mothers had overweightor obesity prior to pregnancy, and 62.3% failed to meet the IOMrecommendations for GWG. Children born to mothers with overweight or obesity exhibitedlower odds of developing eczema at 13 years of age compared tothose born to mothers with underweight or normal weight, withan adjusted odds ratio (aOR) of 0.73 (95% CI: 0.60–0.88) (Table 3). No significant associations were observed between maternal BMI and the other allergic diseases at any of the assessed time points. All analyses for anaphylaxis and food allergy are present in Tables S8–S10. Excessive GWG, based on IOM criteria, was associated with in-creased odds of asthma at both 7 (aOR = 1.30; 95% CI: 1.01–1.66)and 13 years (aOR = 1.29; 95% CI: 1.01–1.65), as well as with rhinitisat 4 years (aOR = 1.48; 95% CI: 1.10–1.98). When GWG was ana- lyzed using z-scores that accounted for gestational age and maternal BMI, children whose mothers were in the highest tertile had greaterodds of asthma at 7 years (aOR = 1.33; 95% CI: 1.03–1.72), rhinitis at4 years (aOR = 1.54; 95% CI: 1.13–2.09), and allergic sensitization at10 years (aOR = 1.44; 95% CI: 1.05–1.97) (Table 4). In contrast, higher GWG was associated with reduced odds ofeczema at age 4 (aOR = 0.81; 95% CI: 0.66–0.998), while lower GWGwas linked to increased odds of eczema at 13 years (aOR = 1.26;95% CI: 1.02–1.56). No significant associations were found betweenGWG and either food allergy or anaphylaxis (Tables S11–S13). Stratified analyses by maternal BMI revealed that among moth- ers with underweight or normal weight, being in the highest tertile of GWG z-score was associated with increased odds of asthma and rhinitis during early childhood, as well as reduced odds of eczema at age 4 and increased odds at age 13 if GWG was in the lowest ter- tile. Among mothers with overweight or obesity, higher and lower GWG was associated with increased odds of allergic sensitizationat 10 years of age (Table 5). Further sensitivity analyses with mater- nal BMI categories (normal weight excluding underweight category vs. overweight/obesity) are presented in (Table S14). Results were overall consistent when excluding underweight mothers, with sim- ilar effect sizes observed.4 | D I S CUS S I O NIn this population-based birth cohort, we found that a higher GWG, when exceeding IOM guidelines or falling in the highest tertile of GWG z-scores, was associated with increased odds of asthma, rhinitis, and allergic sensitization. In contrast, a higher GWG z-score and maternal pre-pregnancy overweight or obesity were associated with reduced odds of eczema, while a lower GWG z-score increased the odds. These findings highlight the complex and condition-specific role of maternal weight, both before and during pregnancy, as an early-life determinant of childhood allergic diseases.4.1 | Maternal pre-pregnancy BMI and allergicdiseasesOur findings suggest that maternal overweight or obesity before pregnancy is associated with lower odds of eczema in offspring at13 years. This observation aligns with previous research, includinga meta-analysis that reported reduced odds of atopic dermatitis in children born to mothers who were overweight or obese prior to pregnancy. 36 However, the authors of that meta-analysis cautioned against interpreting these associations as protective, noting that the inverse relationship did not hold consistently across subgroup analyses considering more robust study designs, different age groups, excluding studies with fewer than 10,000 cases, non-U.S. cohorts, and studies using medical records. 36 Nonetheless, another recent meta-analysis also supports a subtle inverse association, reporting slightly reduced odds of “eczema ever” among children of overweight mothers and a similar but non-significant trend for maternal obesity. 37 A study from 2022 explored the influence of maternal BMI mea- surement methods.38 When stratified by whether pre-pregnancy weight was measured or self-reported, the study found that objec- tively measured maternal obesity was associated with a reduced riskof dermatitis (adjusted hazard ratio [aHR] = 0.93; 95% CI: 0.90–0.97),whereas self-reported obesity showed a slightly increased risk(aHR = 1.05; 95% CI: 1.00–1.10). 38 These findings suggest that reli- ance on self-reported weight may attenuate or obscure associations in some studies. Maternal pre-pregnancy BMI has been inversely associated with cord-blood immunoglobulin E levels, a marker of the immune response of the fetus, and typically increased in eczema.9 These ### Page 5 | 5 of 13RODRIGUES et al.findings point to a potential protective effect of higher maternal BMI against the development of eczema, although the underlying mech- anisms remain unclear. It is also possible that factors associated with maternal overweight may play a mediating role. Our study contrib- utes to this ongoing discussion by providing longitudinal evidence from childhood into adolescence, underscoring the need for future research to disentangle the biological or environmental pathways through which maternal adiposity may influence eczema risk. In our study, we did not find any significant association be- tween pre-pregnancy BMI and other allergic diseases. In two meta-analyses, maternal obesity before pregnancy was associated with higher odds of wheeze and asthma in the offspring, as wasTA B L E 1 Maternal and child characteristics according to pre-pregnancy BMI categories in the generation XXI cohort.Total (n = 7280) Underweight/normal weight(n = 5020, 69%) Overweight/obese(n = 2260, 31.0%) p-valueSex, n (%) 0.295 Female 3567 (49.0) 2439 (48.6) 1128 (49.9)Male 3713 (51.0) 2581 (51.4) 1132 (50.1)Mother age, years, mean ± SD 29.20 ± 5.51 28.79 ± 5.54 30.10 ± 5.33 <0.001Maternal education, n (%) <0.001≤9 years 3416 (47.2) 2118 (42.4) 1298 (57.6) ≥10 e ≤12 1983 (27.4) 1402 (28.1) 581 (25.8)>12 1845 (25.5) 1472 (29.5) 372 (16.6) Parity, multiparous, n (%) 3062 (42.7) 1906 (38.5) 1156 (52.0) <0.001Maternal history of allergic disease, n (%) 1217 (17.4) 825 (17.0) 392 (18.3) 0.161 Maternal smoking in pregnancy, n (%) 1582 (22.1) 1170 (23.7) 412 (18.5) <0.001GWG categories, n (%)a <0.001Insufficient 1732 (25.1) 1413 (29.5) 319 (15.1) Adequate 2604 (37.7) 1992 (41.5) 612 (29.1) Excessive 2565 (37.2) 1390 (29.0) 1175 (55.8)GWG z-score, mean ± SD −0.02 ± 1.18 0.03 ± 1.17 −0.13 ± 1.17 <0.001Asthma, n (%) 4 years 286 (4.3) 192 (4.2) 94 (4.6) 0.508 7 years 402 (6.3) 278 (6.3) 124 (6.2) 0.859 10 years 492 (8.2) 329 (7.9) 163 (8.9) 0.19613 years 415 (9.6) 280 (9.3) 135 (10.2) 0.395 Rhinitis, n (%) 4 years 286 (4.4) 205 (4.5) 81 (4.0) 0.2967 years 504 (7.9) 361 (8.2) 143 (7.1) 0.14513 years 420 (9.7) 304 (10.1) 116 (8.7) 0.142 Eczema, n (%) 4 years 675 (12.7) 499 (13.7) 176 (10.4) <0.0017 years 835 (13.5) 612 (14.4) 223 (11.5) 0.00213 years 673 (15.6) 514 (17.2) 159 (12.0) <0.001Food Allergy, n (%) 13 years 150 (4.4) 108 (4.6) 42 (4.0) 0.372 Anaphylaxis, n (%) 13 years 124 (2.9) 89 (3.0) 35 (2.6) 0.530Sensitization (from 1078 children), n (%) 10 years 432 (40.1) 304 (42.5) 128 (35.4) 0.025Note: Statistically significant results are indicated in bold (p < .05).Abbreviations: GWG, gestational weight gain; SD, standard deviation. a According to the Institute of Medicine recommendations. Chi-square (χ2 ) tests were used to compare differences between categorical variables; independent samples t-tests were used to compare continuous variables between groups. Statistically significant results are indicated in bold (p < .05). ### Page 6 6 of 13 |RODRIGUES et al.maternal overweight.18,37 In our study, asthma was based on pa- rental report of a physician diagnosis. In the metanalysis by Liu et al. associations between maternal BMI and childhood asthma were weaker when asthma was identified through parental report rather than medical diagnosis. In fact, for maternal overweight, the association lost statistical significance. This suggests that relianceTA B L E 2 Maternal and child characteristics according to gestational weight gain categories based on IOM guidelines in the generationXXI cohort.Total of participants (n = 6901)Insufficient GWG(1732, 25.1%)Adequate GWG(2604, 37.7%)Excessive GWG(2565, 37.2%) p-valueSex, n (%) 0.200 Female 3377 (48.9) 872 (50.3) 1283 (49.3) 1222 (47.6) Male 3524 (51.1) 860 (49.7) 1321 (50.7) 1343 (52.4)Mother age, years, mean ± SD 29.20 ± 5.47 29.56 ± 5.76 29.33 ± 5.41 28.84 ± 5.31 <0.001Maternal education, n (%) <0.001≤9 years 3202 (46.5) 859 (49.7) 1141 (44.0) 1202 (47.0)≥10 e ≤12 1890 (27.5) 405 (23.4) 726 (28.0) 759 (29.6)>12 1791 (26.0) 466 (26.9) 726 (28.0) 599 (23.4) Parity, multiparous, n (%) 3062 (42.7) 805 (47.0) 1110 (43.2) 977 (38.7) <0.001Maternal history of allergic disease,n (%)1195 (17.4) 306 (17.7) 437 (16.9) 452 (17.8) 0.656 Maternal smoking in pregnancy, n (%) 1507 (22.1) 335 (19.6) 514 (19.9) 658 (26.2) <0.001Mother BMI, n (%)a <0.001Underweight 264 (3.8) 108 (6.2) 112 (4.3) 44 (1.7) Normal weight 4531 (65.7) 1305 (75.3) 1880 (72.2) 1346 (52.5) Overweight 1495 (21.7) 178 (10.3) 458 (17.6) 859 (33.5)Obesity 611 (8.9) 141 (8.1) 154 (5.9) 316 (12.3) Mother BMI, kg/m 2, mean ± SD 23.89 ± 4.23 23.31 ± 4.46 23.28 ± 3.85 24.89 ± 4.26 <0.001Z-score, mean ± SD −0.20 ± 1.18 −1.39 ± 0.80 −0.15 ± 0.48 1.03 ± 0.82 0.001Asthma, n (%) 4 years 273 (4.4) 69 (4.4) 88 (3.7) 116 (5.0) 0.088 7 years 388 (6.4) 101 (6.6) 127 (5.5) 160 (7.0) 0.085 10 years 467 (8.2) 99 (7.1) 172 (7.9) 196 (9.3) 0.04713 years 394 (9.6) 95 (9.5) 134 (8.4) 165 (10.9) 0.066 Rhinitis, n (%) 4 years 276 (4.4) 66 (4.2) 88 (3.7) 122 (5.3) 0.0327 years 484 (7.9) 113 (7.4) 183 (7.9) 188 (8.3) 0.64413 years 400 (9.7) 101 (10.1) 156 (9.8) 143 (9.4) 0.695 Eczema, n (%) 4 years 648 (12.8) 162 (12.8) 261 (13.7) 225 (12.0) 0.3247 years 805 (13.7) 193 (13.3) 328 (14.7) 284 (12.8) 0.16913 years 644 (15.7) 177 (17.8) 245 (15.4) 222 (14.7) 0.103 Food allergy, n (%) 13 years 146 (4.6) 34 (4.6) 60 (4.9) 52 (4.2) 0.684Anaphylaxis, n (%) 13 years 121 (2.9) 26 (2.6) 54 (3.4) 41 (2.7) 0.389Sensitization (from 1019 children), n (%) 10 years 405 (39.7) 89 (40.1) 144 (39.2) 172 (40.0) 0.969Note: Chi-square (χ2 ) tests were used for categorical variables; one-way ANOVA was used for comparisons involving continuous variables across groups with three or more categories. Statistically significant results are indicated in bold (p < .05).Abbreviations: BMI, body mass index; SD, standard deviations. a According to WHO criteria. ### Page 7 | 7 of 13RODRIGUES et al.on parental report may attenuate true associations due to potential misclassification of asthma.18A recent large study by Rosenquist et al., 39 analyzed nearly100,000 mother–child pairs using electronic medical records.Asthma was defined based on International Classification of Diseases diagnostic codes and asthma medication dispensing, ensuring high specificity. The study reported small increases in asthma risk across maternal BMI categories, some of which did not reach statistical sig- nificance. 39 Likewise, a recent cohort study found no associations between early-pregnancy BMI and physician-diagnosed asthma (val- idated through medication reimbursement data). 32 Together, these studies suggest that results may differ depending on the definition and ascertainment of asthma, which may partly explain the null find- ings observed in our cohort. 32,39 Similarly to our study, in the meta-analysis by Zhang et al. ma- ternal overweight and maternal obesity before pregnancy were not associated with an increased risk of rhinitis in the offspring. 37 As for allergic sensitization, two prospective cohort studies, comparable to ours, found no associations between early-pregnancy BMI and aller- gic sensitization measured by IgE levels.8,324.2 | Maternal GWG and allergic diseasesOur findings indicate that excessive GWG, as defined by the IOM, is associated with increased odds of asthma in offspring at both 7and 13 years of age, as well as increased odds of rhinitis at 4 years.When GWG was examined using z-scores– accounting for maternalBMI and gestational age– children whose mothers were in the high- est tertile of GWG z-score had significantly greater odds of havingasthma at 7 years, of rhinitis at 4 years, and of allergic sensitizationat 10 years of age.These results align with previous studies reporting a positive association between higher GWG and allergic diseases, particularly asthma.3,7,11,18,20 A meta-analysis suggested that each 1 kg increasein GWG was associated with a 1.5% increase in childhood asthmaor wheezing odds. 3 Although that meta-analysis included hetero- geneous GWG definitions and did not use IOM categories, pooled results from high GWG groups consistently indicated elevated odds. 3 A more recent meta-analysis further supported these find-ings, showing increased odds of asthma with GWG above 20 kg.18However, in two meta-analyses, when examining studies using IOM-defined categories, excessive GWG was not significantly associated with asthma,18,37 possibly reflecting the limited number of studies using this definition. Individual cohort and cross-sectional studies further support this findings. The Danish National Birth Cohort reported thatGWG ≥25 kg was associated with nearly double the odds of severeasthma.11 Although no link with hay fever was found in that cohort, the Shanghai Children Allergy Study, a large cross-sectional studyof over 15,000 mother–child pairs, found that excessive GWG, asdefined by the IOM, increased the risk of both asthma and allergic rhinitis. 20 Considering allergic sensitization, our results indicate a sig- nificant positive association with GWG z- score, which aligns with findings from the Shanghai study where mothers with GWG above IOM recommendations had increased prevalence ra- tios for sensitization. 20 In contrast, a Finnish birth cohort found no association between GWG and sensitization. 32 However, that study used weekly weight gain categories that did not accountTA B L E 3 Associations between maternal pre-pregnancy BMI categories and offspring allergic diseases from childhood to adolescence.nAsthmaaOR (95% CI) nRhinitis aOR(95% CI) nEczemaaOR (95% CI) nAllergic sensitizationaOR (95% CI)4 years 6606 6571 5322 - -Maternal underweight/normal weight 4552 Reference 4526 Reference 3632 Reference - -Maternal overweight/obesity 2054 1.09(0.84–1.41)2045 1.01(0.77–1.32)1690 0.84(0.70–1.02)- -7 years 6430 6413 6206 - -Maternal underweight/normal weight 4421 Reference 4408 Reference 4263 Reference - -Maternal overweight/obesity 2009 0.95(0.76–1.19)2005 0.90(0.73–1.11)1943 0.91(0.77–1.08)- -10 years 5985 - - - - 1078Maternal underweight/normal weight 4156 Reference - - - - 716 Reference Maternal overweight/obesity 1829 1.13(0.92–1.38)- - - - 362 0.77 (0.59–1.02) 13 years 4329 4327 4313 - -Maternal underweight/normal weight 3000 Reference 2996 Reference 2988 Reference - -Maternal overweight/obesity 1329 1.07(0.86–1.34)1331 0.91(0.72–1.15)1325 0.73 (0.60–0.88)- -Note: Logistic Regression Model adjusted for sex of the children, maternal education, maternal age, smoking during pregnancy, maternal history ofallergic diseases, and parity. Statistically significant results are indicated in bold (p < .05). ### Page 8 8 of 13 |RODRIGUES et al.for pre-pregnancy BMI and gestational age, which may have obscured differences. Interestingly, we also observed that higher GWG z-score wasassociated with lower odds of eczema at 4 years, while lower GWGz-score was linked to higher odds of eczema at 13 years. Prior liter- ature on this topic has been inconsistent. One meta-analysis foundthat GWG above 15–25 kg was associated with a higher risk of atopicdermatitis, as was excessive GWG by IOM criteria. 36 However, a more recent meta-analysis based on IOM categories did not repli- cate these findings. 37 Moreover, the Shanghai study found lower odds of eczema in children whose mothers gained less than the IOM recommendation, 20 while the U.S.-based Growing Up Today Study reported no significant associations.14 These discrepancies likely reflect differences in how GWG was defined. Studies using crude weight thresholds (e.g., <10 kg or >25 kg) may not adequately ac- count for gestational age or maternal BMI. The use of GWG z-scores,TA B L E 4 Associations between gestational weight gain (IOM categories and Z-scores) and offspring allergic diseases at ages 4, 7, 10, and13 years.nAsthma aOR(95% CI) nRhinitis aOR(95% CI) nEczema aOR(95% CI) nAllergic sensitizationaOR (95% CI)4 years 6268 6234 5049 - -IOM, Insufficient a 1560 1.21 (0.87–1.68) 1553 1.17 (0.84–1.63) 1267 0.95 (0.77–1.18) - -IOM, Adequate a 2386 Reference 2369 Reference 1911 Reference - -IOM, Excessive a 2322 1.33 (0.99–1.79) 2312 1.48 (1.10–1.98) 1871 0.89 (0.73–1.09) - -GWG z-score, continuous 6263 1.06 (0.95–1.17) 6229 1.09 (0.98–1.22) 5047 0.96 (0.89–1.03) - -GWG z-score, 1st tertile 2139 0.80 (0.59–1.10) 2133 1.30 (0.95–1.78) 1741 0.88 (0.72–1.07) - -GWG z-score, 2nd tertile 2065 Reference 2049 Reference 1668 Reference - -GWG, z-score, 3rd tertile 2059 1.09 (0.82–1.47) 2047 1.54 (1.13–2.09) 1638 0.81 (0.66–0.998)- -7 years 6107 6094 5893 - -IOM, Insufficient a 1523 1.21 (0.92–1.59) 1517 0.92 (0.72–1.18) 1454 0.90 (0.74–1.10) - -IOM, Adequate a 2313 Reference 2309 Reference 2228 Reference - -IOM, Excessive a 2271 1.30 (1.01–1.66) 2268 1.08 (0.87–1.35) 2211 0.86 (0.72–1.03) - -GWG z-score, continuous 6102 1.06 (0.97–1.16) 6089 1.05 (0.96–1.14) 5888 0.97 (0.90–1.03) - -GWG z-score, 1st tertile 2086 1.03 (0.79–1.34) 2081 1.09 (0.86–1.38) 1994 0.99 (0.83–1.20) - -GWG z-score, 2nd tertile 2011 Reference 2003 Reference 1936 Reference - -GWG, z-score, 3rd tertile 2005 1.33 (1.03–1.72) 2005 1.25 (0.99–1.57) 1958 0.90 (0.75–1.09) - -10 years 5695 - - - - 1019 IOM, Insufficient a 1401 0.89 (0.69–1.15) - - - - 222 1.00 (0.71–1.42)IOM, Adequate a 2187 Reference - - - - 367 Reference IOM, Excessive a 2107 1.15 (0.92–1.43) - - - - 285 1.10 (0.81–1.49)GWG z-score, continuous 5693 1.08 (0.99–1.17) - - - - 1019 1.07 (0.95–1.20)GWG z-score, 1st tertile 1949 0.87 (0.68–1.11) - - - - 318 1.11 (0.80–1.54)GWG z-score, 2nd tertile 1862 Reference - - - - 326 Reference GWG, z-score, 3rd tertile 1882 1.16 (0.92–1.46) - - - - 375 1.44 (1.05–1.97)13 years 4111 4108 4097 - -IOM, Insufficient a 1002 1.13 (0.86–1.49) 999 1.02 (0.78–1.33) 996 1.18 (0.95–1.47) - -IOM, Adequate a 1592 Reference 1589 Reference 1586 Reference - -IOM, Excessive a 1517 1.29 (1.01–1.65) 1520 0.97 (0.76–1.25) 1515 1.01 (0.82–1.24) - -GWG z-score, continuous 4111 1.03 (0.94–1.13) 4108 0.95 (0.87–1.05) 4097 0.96 (0.88–1.03) - -GWG z-score, 1st tertile 1405 1.12 (0.86–1.45) 1402 1.14 (0.88–1.47) 1398 1.26 (1.02–1.56) - -GWG z-score, 2nd tertile 1364 Reference 1363 Reference 1362 Reference - -GWG, z-score, 3rd tertile 1342 1.22 (0.94–1.59) 1343 1.19 (0.92–1.54) 1337 1.13 (0.91–1.40) - -Note: Logistic Regression Models adjusted for sex of the children, maternal education, maternal pre-pregnancy BMI, maternal age, smoking during pregnancy, maternal history of allergic diseases, parity. Tertiles of GWG z-score: 1st: ≤ −0.48; 2nd: > −0.48 and ≤0.43; 3rd: >0.43. Statistically significant results are indicated in bold (p < .05).Abbreviations: GWG, gestational weight gain; IOM, institute of medicine. a According to the Institute of Medicine Guidelines for Gestational Weight Gain. ### Page 9 | 9 of 13RODRIGUES et al.TA B L E 5 Associations between gestational weight gain Z-score tertiles and offspring allergic diseases stratified by maternal pre-pregnancy BMI.GWG z-score nAsthma aOR(95% CI) nRhinitis aOR (95% CI) nEczema aOR(95% CI) nAllergic SensitizationaOR (95% CI)4 yearsMaternal underweight/normalweight 1st tertile 1434 0.93 (0.63–1.38) 1429 1.63 (1.10–2.42) 1157 0.88 (0.69–1.11) - -2nd tertile 1385 Reference 1369 Reference 1106 Reference - -3rd tertile 1533 1.35 (0.95–1.93) 1527 2.07 (1.42–3.01) 1201 0.78 (0.61–0.99) - -Maternal overweight/obesity 1st tertile 705 0.63 (0.37–1.05) 704 0.86 (0.50–1.48) 584 0.87 (0.59–1.29) - -2nd tertile 680 Reference 680 Reference 562 Reference - -3rd tertile 526 0.70 (0.40–1.21) 520 0.76 (0.42–1.36) 437 0.93 (0.62–1.39) - -7 years - -Maternal underweight/normalweight 1st tertile 1401 1.16 (0.84–1.60) 1398 1.14 (0.86–1.51) 1335 0.93 (0.75–1.15) - -2nd tertile 1345 Reference 1338 Reference 1291 Reference - -3rd tertile 1484 1.39 (1.02–1.89) 1483 1.36 (1.03–1.79) 1453 0.88 (0.71–1.09) - -Maternal overweight/obesity 1st tertile 685 0.79 (0.49–1.22) 683 1.02 (0.67–1.56) 659 1.17 (0.83–1.65) - -2nd tertile 666 Reference 665 Reference 645 Reference - -3rd tertile 521 1.25 (0.80–1.97) 522 1.02 (0.65–1.60) 505 0.97 (0.67–1.41) - -10 yearsMaternal underweight/normalweight 1st tertile 1315 0.82 (0.60–1.11) - - - - 204 0.87 (0.58–1.31)2nd tertile 1259 Reference - - - - 205 Reference 3rd tertile 1406 1.26 (0.95–1.66) - - - - 270 1.33 (0.91–1.94)Maternal overweight/obesity 1st tertile 634 0.96 (0.64–1.44) - - - - 114 1.78 (1.01–3.12)2nd tertile 603 Reference - - - - 121 Reference 3rd tertile 476 0.93 (0.60–1.43) - - - - 105 1.86 (1.02–3.40)13 yearsMaternal underweight/normalweight 1st tertile 949 1.10 (0.79–1.52) 946 1.16 (0.85–1.59) 945 1.30 (1.02–1.65) - -2nd tertile 914 Reference 913 Reference 911 Reference - -3rd tertile 1002 1.28 (0.94–1.75) 1002 1.27 (0.94–1.72) 998 1.09 (0.86–1.40) - -Maternal overweight/obesity 1st tertile 456 1.17 (0.75–1.83) 456 1.07 (0.67–1.72) 453 1.18 (0.78–1.80) - -2nd tertile 450 Reference 450 Reference 451 Reference - -3rd tertile 340 1.11 (0.68–1.79) 341 0.99 (0.59–1.65) 339 1.29 (0.84–2.01) - -Note: Logistic Regression Model adjusted for sex of the children, maternal education, maternal age, smoking during pregnancy, maternal history of allergic diseases, parity. Tertiles of GWG z-score: 1st: ≤−0.48; 2nd: > −0.48 and ≤0.43; 3rd: >0.43. Statistically significant results are indicated in bold (p < .05). ### Page 10 10 of 13 |RODRIGUES et al.which integrate both, may provide a more individualized measure of weight gain adequacy and may capture associations that IOM cut- offs miss. When we stratified our analysis by maternal BMI category, the increased eczema risk associated with lower GWG was only ob- served among mothers with underweight or normal BMI. This sug- gests that low GWG may be more detrimental in pregnancies with limited maternal reserves, which may predispose to suboptimal fetal nutrition or altered immune system development. Taken together, our results add to a growing body of evidence suggesting that, overall, an inadequate GWG, low or high, may influ- ence the risk of allergic diseases in offspring. Several mechanisms may underlie these associations. Excessive GWG has been linked to a pro-inflammatory state in pregnancy, characterized by elevated cytokines such as TNF-α and C-reactive protein (CRP).40–42 One study found that children of mothers in the highest GWG tertile had elevated TNF-α in early life, which in turn was associated with a higher risk of asthma.40 Other research has shown that excessive GWG is asso- ciated with increased maternal CRP levels, which have been linked to wheezing and respiratory infections in offspring.41,42 A different hypothesis is that the onset of allergic diseases could be connected to excessive GWG through the exposure of the fetus to poor dietary pat- terns during pregnancy, which are often connected to more energy-dense foods and consequently may cause excessive GWG. 43 In fact, a healthier diet during pregnancy has been shown to decrease the odds of asthma in offspring.44 Excessive GWG also appears to negatively influence infants' gut microbiota, decreasing the alpha diversity and abundance of neonatal gut microbiota.45 In turn, a low alpha diversity has been associated with an increased risk of allergic diseases.46 Interestingly, maternal obesity has been associated with lower cord blood IgE levels, whereas eczema is typically linked to elevated IgE.9 This may suggest that maternal obesity or high GWG may mod- ify fetal immune development in a way that reduces IgE-mediated pathways during perinatal life, possibly lowering the risk of eczema. However, other allergic conditions may still be promoted through IgE-independent mechanisms, driven by systemic inflammation and immune dysregulation in later life. Overall, our findings support the hypothesis that excessive GWG may promote allergic disease development through inflammatory, metabolic, and microbial pathways (Figure 1). On the other hand, insufficient weight gain may also be deleterious to the offspring, causing suboptimal development. These effects may be amplified or modified by maternal BMI, highlighting the importance of per- sonalized GWG guidance based on pre-pregnancy nutritional status. Further research is needed to clarify causality and mechanisms, but from a public health perspective, our results reinforce the value of promoting healthy weight gain during pregnancy as a potential strat- egy for reducing allergy risk in the next generation.4.3 | Strenghts and limitationsThe limitations of this study should be acknowledged. First, pre-pregnancy weight was primarily self-reported, which may intro- duce recall bias and misclassification. However, previous research indicates strong agreement between self-reported and measuredweights, particularly when recall occurs within 1 year postpartum,as in our study. 47 Moreover, only total GWG was considered with no trimester-specific measurements available. Even if gestational age was accounted for when using the GWG z-scores, the trajectory of GWG may be a relevant factor in this association. 22 Additonally, we could not account for other potential nutritional factors dur- ing pregnancy that may have contributed to greater GWG and, in turn, allergic diseases. 43 It is also important to recognize that the mechanisms underlying each allergic disease may differ. While ma- ternal adiposity may influence immune and growth-related path- ways, genetic factors, such as filaggrin mutations, play a major role in skin barrier dysfunction and susceptibility to eczema. Information on filaggrin mutations or other genetic variants was not available in our cohort. Moreover, diagnoses of allergic diseases were based on parental reports of physician diagnoses, which may be prone to misclassification. In addition, we did not distinguish between asthma phenotypes nor account for asthma severity; nonetheless, this approach is commonly used in epidemiological studies and likely results in non-differential bias, which tends to attenuate associa- tions.48 Additionally, paternal history of allergic disease and smoking exposure in infancy were not included due to limited data availabilityF I G U R E 1 Pathways through which maternal nutritional status indicators may influence allergic diseases. ### Page 11 | 11 of 13RODRIGUES et al.and low prevalence, respectively. Finally, as with all observational studies, residual confounding cannot be entirely ruled out, although we used a DAG to guide careful covariate selection. Notwithstanding these limitations, our study has several strengths. We leveraged data from a large, prospective, population-based birth cohort with repeated follow-up assessments extending into adolescence, enabling us to explore allergic outcomes at multi- ple developmental stages, with an extended follow up time. We also examined six distinct allergic outcomes (asthma, rhinitis, eczema, food allergy, anaphylaxis, and allergic sensitization), allowing us to assess the consistency of associations across different immune-mediated conditions. Moreover, although allergic outcomes are bi- ologically related, correlations between conditions in our data were tested and they were consistently weak (coefficients ranging from 0.065 to 0.221), supporting their analysis as distinct outcomes. Furthermore, we tested potential interactions of GWG with ma- ternal BMI and GWG and maternal BMI with child's sex, providing additional insight into the complexity of these associations. The use of standardized validated questionnaires and objective measures of allergic sensitization adds robustness to outcome assessment. We employed both IOM-based GWG categories and GWG z-scores con- sidering gestational age and pre-pregnancy BMI, allowing for a more individualized and biologically relevant analysis of weight gain ade- quacy. Moreover, our stratified analyses by maternal BMI categories provided additional insights into how pre-pregnancy nutritional sta- tus may modify the relationship between GWG and allergic disease. Finally, despite losses to follow-up, effect size analyses comparing included and excluded participants' characteristics indicated only minor differences. Together, these methodological strengths en- hance the relevance of our findings and contribute to the growing body of evidence supporting the importance of maternal health be- fore and during pregnancy in shaping long-term allergic outcomes in children.5 | CO N C LUS I O NOur findings suggest that maternal weight before and during preg- nancy influences the development of allergic diseases in children, with differing effects for eczema, asthma, rhinitis, and allergic sensitization.AU T H O R CO N T R I B U T I O N SMónica Rodrigues: Conceptualization; methodology; data curation;investigation; formal analysis; visualization; writing – original draft;writing – review and editing. Susana Santos: Conceptualization;methodology; investigation; formal analysis; writing – originaldraft; writing – review and editing; supervision. Pedro Moreira:Conceptualization; supervision; writing – original draft; writing – re- view and editing. Francisca Castro Mendes: Writing – review andediting. André Moreira: Conceptualization; supervision; writing –original draft; writing – review and editing.AC K N OW L E D G M E N T SWe gratefully acknowledge the families enrolled in Generation XXIfor their kindness, the participating hospitals and their staff for their help and support, and all previous and current research and field team members for their enthusiasm and perseverance. Open access publication funding provided by FCT (b-on).F U N D I N G I N FO R M AT I O NG21 was funded by Programa Operacional de Saúde – Saúde XXI,Quadro Comunitário de Apoio III and Administração Regional de Saúde Norte (Regional Department of Ministry of Health). This work was supported by FCT Fundação para a Ciência e Tecnologia, I.P. through the projects with references UIDB/04750/2020 and LA/P/0064/2020 and DOI identifiers https://doi.org/10.54499/UIDB/04750/2020 and https://doi.org/10.54499/LA/P/0064/2020. This work was supported by the Portuguese Foundation forScience and Technology–FCT–project reference 2023.02362.BD:10.54499/2023.02362.BD and DOI identifier: https://doi.org/10.54499/2023.02362.BD. SS was supported by the European Union's Horizon Europe Research and Innovation Programme under the Marie Sklodowska-Curie Postdoctoral Fellowship Grant Agreement No. 101109136 (URBANE). Views and opinions expressed are how- ever those of the authors only and do not necessarily reflect those of the European Union or the European Research Executive Agency (REA). Neither the European Union nor the granting authority can be held responsible for them.CO N FL I C T O F I N T E R E S T S TAT E M E N TNo conflicts of interest to report.P E E R R E V I E WFor transparency, the peer review documents associated with this article are available at https://doi.org/10.1111/pai.70357.DATA AVA I L A B I L I T Y S TAT E M E N TThe data from Generation XXI are not publicly available due toprivacy or ethical restrictions. The data can be made available forresearch proposals to the Generation XXI Executive Committee (gen- erationxxi@ispup.up.pt) upon request. Further information aboutGeneration XXI can be obtained via the Generation XXI websitewww.geracao21.com or by emailing generationxxi@ispup.up.pt.O R C I DMónica Rodrigues https://orcid.org/0000-0002-7932-9460R E F E R E N C E S1. Asher MI, Montefort S, Björkstén B, et al. 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