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Background: A novel maternal diet index (MDI), characterizing offspring asthma- and allergy-associated maternal intake during pregnancy was constructed and validated in Healthy Start, USA. This study aims to (1) externally validate the asthma findings from Healthy Start in the NorthPop Birth Cohort Study (NorthPop) in Sweden; and (2) characterize the diet and demographics of the two cohorts.

Methods: The MDI was computed as a weighted combination of seven components associated with offspring allergies and asthma, including vegetables and yogurt (associated with decreased odds) and cold cereals, fried potatoes, juice, red meat, and rice (associated with increased odds). Doctor diagnoses provided childhood asthma incidence and timing. Parametric Weibull time-to-event analysis evaluated associations between the MDI, dichotomized at the median (72.2) for Healthy Start, and offspring asthma.

Results: The NorthPop and Healthy Start mean MDI values differed significantly (p < 0.001) and in NorthPop, only 6.1% had MDI < 72.2. Data from 6446 mother-child dyads in NorthPop yielded a crude hazard ratio (HR) for asthma of 0.70 (95% confidence interval [CI] 0.50–0.98, p = 0.037) and a fully adjusted HR of 0.84 (0.55–1.29; p = 0.428) for MDI > 72.2 versus < 72.2 (n = 4655). The fully adjusted HR for 945 Healthy Start dyads was significant at HR 0.41 (0.29–0.57; p < 0.0001).

Conclusions: Results show that in a population with different maternal dietary patterns and demographics compared to the source population, MDI > 72.2 was not an independent predictor of offspring asthma. Further proof of the utility and generalizability of the MDI needs to be tested in other populations.

Introduction: Diet diversity (DD) in infancy may be protective for early food allergy (FA) but there is limited knowledge about how DD incorporating consumption frequency influences FA risk.

Methods: Three measures of DD were investigated in 2060 infants at 6 and/or at 9 months of age within the NorthPop Birth Cohort Study: a weighted DD score based on intake frequency, the number of introduced foods, and the number of introduced allergenic foods. In multivariable logistic regression models based on directed acyclic graphs, associations to parentally reported physician-diagnosed FA at age 9 and 18 months were estimated, including sensitivity and stratified analyses.

Results: High weighted DD scores (24-31p) at age 9 months were associated with 61% decreased odds of FA at age 18 months [OR (95% CI) = 0.39 0.18–0.88] compared with infants with the lowest DD scores (0-17p). The association remained significant after exclusion of early FA cases. Having introduced 13–14 foods at age 9 months, independent of consumption frequency, was associated with 45% decreased odds of FA [OR (95% CI) = 0.55 (0.31–0.98)] compared to having introduced 0–10 foods. When stratifying, significantly reduced odds for FA were seen for children with eczema and for children with no FA history in the family. No association was seen between DD at age 6 months and FA at age 18 months.

Conclusion: A diverse diet at age 9 months may prevent FA at age 18 months. Our results underscore the need for additional investigations on the impact of consumption frequency in infancy.

Aim: To investigate possible differences in neurodevelopment between lockdown-exposed and non-exposed 18-month-old toddlers in Sweden.

Methods: Data were extracted from the prospective NorthPop Birth Cohort Study in Sweden. Neurodevelopment was assessed using the Ages and Stages Questionnaire Third Edition (ASQ-3) and a clinical routine evaluation at the child health care centre for additional validation. Statistical analyses were performed using IBM SPSS Statistics.

Results: More lockdown-exposed toddlers fell below the cut-off score on the ASQ-3 “Gross motor function” assessment at 18 months, compared to the pre-lockdown category (5.1% vs. 3.6%, adjusted p = 0.002). Conversely, fewer lockdown-exposed toddlers failed the fine motor task “Can draw scribble” versus the pre-lockdown category (1.4% vs. 2.4% adjusted p = 0.014).

Conclusions: Toddlers who were lockdown-exposed had lower gross motor function but were more successful in the fine motor task at 18 months.

Background: Epigenetic alterations during fetal development have been proposed as key factors explaining associations between maternal lifestyle during pregnancy and later health outcomes in the offspring, pertaining to the developmental origin of health and disease hypothesis.

Objectives: To assess the association of maternal lifestyle with offsprings’ birth weight and underlying epigenetic mediatory mechanisms in the NorthPop prospective birth cohort.

Methods: A three-step analytic pipeline was applied. In 722 mother–child pairs, overall associations between ten maternal lifestyle factors and the offspring’s standardized birth weight were first evaluated by multiple linear regression. Three high-dimensional mediation methods, based on sure independence screening and penalized regression, were then applied on the beta methylation matrix to identify candidate CpG mediators in cord blood driving the significant overall associations. Finally, robust and ordinary least squares (OLS) regression-based classical mediation methods were used with candidate CpG probes to assess single- and multiple (parallel and serial)-mediator models on a low-dimensional space.

Results: Gestational weight gain (GWG) (β-adj = 0.03; p = 2 × 10–5) and maternal BMI at the beginning of pregnancy (β-adj = 0.036; p = 1 × 10–4) were significantly associated with the offspring’s standardized birth weight. High-dimensional mediation analyses identified pooled sets of four (cg19242268 [TCEA2]; cg08461903 [N/A]; cg14798382 [CHERP/C19orf44] and cg21516291 [SLC35C2]) and five (cg17040807 [CYGB]; cg19242268 [TCEA2]; cg26552621 [CIRBP]; cg04457572 [CDH23] and cg06457011 [PLCG1]) candidate CpG mediators related to GWG and BMI at the beginning of pregnancy, respectively. For both exposures, classical mediation analyses revealed a range of significant single- and multiple (both serial and parallel)-mediator models via both robust and OLS regression based approaches. These indicated the likely presence of individual, causally linked multiple, and causally independent multiple mediatory pathways underlying the two significant overall associations.

Conclusions: Our findings support the hypothesis that neonatal health effects related to maternal lifestyle may be partly mediated by epigenetic alterations. Findings also suggest the possible involvement of multiple DNA methylation sites via various mediatory pathways.

Background: Maternal diet during pregnancy is considered a potential modifiable risk factor for allergic diseases in offspring. The dietary inflammatory index (DII) is a tool to assess the inflammatory potential of the diet and has been suggested to be associated with offspring allergy development. Its association with food allergy and immunoglobulin E (IgE) sensitization in children remains understudied.

Methods: This study analyzed 4709 mother-partner-child triads from the NorthPop Birth Cohort in Sweden. Maternal DII scores were calculated from a food frequency questionnaire administered at gestational week 34. Allergy outcomes at 18 months included parent-reported physician-diagnosed food allergy, parent-reported eczema and atopic eczema according to UK Working Party criteria, parent-reported ever wheeze, parent-reported physician-diagnosed asthma, and IgE sensitization to food and airborne allergens. Associations between maternal DII scores (continuous and quartiles) and allergic outcomes were assessed using logistic regression, adjusting for maternal age, allergic heredity, farm living, region of birth, siblings, and education.

Results: At age 18 months, 4.9% of children had physician-diagnosed food allergy, 30.6% had eczema, 11.4% had atopic eczema, 15.9% reported ever wheeze, 4.1% had physician-diagnosed asthma, and 19% were IgE sensitized. No significant associations were found between maternal DII scores and the allergic outcomes of interest.

Conclusion: This large birth cohort study found no association between maternal DII during pregnancy and allergic diseases or IgE sensitization in 18-month-old children, suggesting that a proinflammatory diet during pregnancy does not influence early allergic outcomes. Further research is needed to clarify the role of maternal diet in offspring immune development.

Background: Non-communicable diseases (NCDs) are a global health issue, posing a substantial burden on the individual, community, and public health. The risk of developing NCDs is influenced by a complex interplay between genetic, epigenetic, and environmental factors.

Methods: The NorthPop Birth Cohort Study (NorthPop) constitutes an infrastructure enabling cutting-edge research on the foundational pathways to NCDs in childhood, including allergic diseases and asthma, overweight/obesity, cognitive and neurodevelopmental dysfunction, gastrointestinal disorders, and caries. NorthPop aims at recruiting 10,000 families. Pregnant women and their partners residing in Västerbotten County, Sweden are eligible. Recruitment started in 2016 and is anticipated to end in 2025. Extensive data on parental, fetal and child health outcomes, lifestyle, diet, and environmental exposures are prospectively collected using web-based questionnaires in pregnancy and childhood until the children turn 7 years old. Urine samples are collected from the pregnant woman at gestational age 14–24 weeks. Blood samples are collected at gestational age 28 weeks. Placenta and cord blood are collected at birth. A breast milk sample is collected 1 month postpartum. Blood samples from the children are collected at 18 months and 7 years of age. Oral swabs and fecal samples are collected from the children within 48 h of birth, at 1, 9 and 18 months, 3 and 7 years of age. At age 7 years, children are invited to a follow-up visit, including measurements of weight, height, blood pressure, pulse, hand grip strength, working memory, skin prick test and saliva sampling. Additional measurements, such as sleep–wake and light exposure, and additional biological samples are collected in sub-cohorts. Permission for linkage to medical records and national registers e.g., the Swedish Pregnancy Register, the National Patient Register, the Longitudinal Integration Database for Health insurance and Labor market studies and the Swedish Prescribed Drug Register has been granted.

Discussion: Our multidisciplinary approach allows us to study how early life exposures, as well as parental health and lifestyle, influence future health in the offspring. Our results are anticipated to contribute to the understanding of disease risk and may inform future strategies aimed at risk reduction, highly significant for public health.

Trial registration: Retrospectively registered at Researchweb 11 November 2024 (project number 279272).

Concerns have been raised that an overconsumption of baby food fruit pouches among toddlers might increase the risk of childhood obesity. This study aimed to quantify the consumption of fruit pouches and other fruit containing food products and to explore potential correlations between the consumption of these products and body-mass index z-score (BMIz) at 18 months, taking other predictive factors into consideration. The study was based on 1499 children and one-month-recall food frequency questionnaires from the Swedish population-based birth cohort NorthPop. Anthropometric outcome data were retrieved from child health care records. BMIz at 18 months of age was correlated to maternal BMI and gestational weight gain and inversely correlated to fruit juice consumption and breastfeeding. BMIz at 18 months of age was not correlated to consumption of fruit pouches, sugar-sweetened beverages, whole fruit or milk cereal drink. Overweight at 18 months of age was correlated to maternal BMI and inversely correlated to breastfeeding duration. To our knowledge, this is the first study that investigates possible associations between baby food fruit pouch consumption and overweight in toddlers. We found that moderate fruit pouch consumption is not associated with excess weight at 18 months of age.