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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.

Background/Objectives: The complementary feeding period is a critical window for shaping infant diet, gut microbiota, and immune development. While allergic symptoms often emerge in the first year of life, the effects of specific foods, such fruits, on infant allergy symptoms, inflammation, immunity and associated microbiota remain unclear. This study aimed to assess the impact of daily blueberry consumption during the complementary feeding period on allergy-related symptoms, immune biomarkers, and gut microbiota in breastfed U.S. infants.

Methods: In a double-blind, randomized, placebo-controlled trial, infants from the Denver metro area were assigned to receive up to 10 g/day of freeze-dried blueberry powder or an isocaloric placebo from 5 to 12 months of age. Stool, blood, and caregiver-reported allergy-related symptom data were collected at baseline and study end.

Results: Of the 76 infants enrolled, 61 completed the study (Blueberry: n = 30; Placebo: n = 31). While more infants in the blueberry group had allergy-related symptoms at baseline, they had significantly different longitudinal symptom trajectories than the placebo (p = 0.05), showing a greater resolution rate of symptoms by study end. Pro-inflammatory serum IL-13 levels were significantly reduced (p = 0.035) and anti-inflammatory IL-10 levels borderline increased (p = 0.052) in the blueberry group. However, changes in allergy symptoms were not significantly associated with IL-10 or IL-13. The relative abundances of Lacticaseibacillus, Blautia, and Peptostreptococcaceae at 12 months were negatively correlated with IL-10, while Lactobacillus, Clostridiaceae, and Megasphaera were positively associated. IL-13 was positively associated with Citrobacter and negatively associated with Anaerostipes and Blautia.

Conclusions: The consumptio9n of blueberries as an early complementary food may improve resolution of allergy symptoms, modulate immune biomarkers, and promote beneficial shifts in gut microbiota during infancy. Future research should aim to identify the specific bioactive components of blueberries responsible for these effects and explore the potential of other complementary foods to favorably influence developing biological systems involved in microbiota and immune development.

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.

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.

Individual studies indicate that maternal diet during pregnancy may be associated with child allergy outcomes. We performed a systematic review to summarize the available data focusing on overall maternal dietary intake rather than single foods and nutrients. Searches included PubMed, OVID Medline, Web of Science, and Embase up to November 28, 2024. Searches were not restricted by geographical location and included studies published in English only. The ROBINS-I Cochrane tool was used to assess risk of bias. Meta-analysis was conducted when ≥2 studies examined the same dietary pattern-outcome-age combination; a fixed- or random-effects model was used based on I2. When studies reported multiple effect sizes, a multilevel meta-analysis accounted for within-study clustering. We included 28 papers reporting on 29 diet patterns, indices, or diversity. Diet patterns included healthy and unhealthy diet patterns, healthy and unhealthy diet indices, and healthy and unhealthy diet diversity. Allergy outcomes were atopic dermatitis/eczema, food allergy, allergic rhinitis, asthma, and allergic sensitization/atopy. Only diet diversity during pregnancy showed a modest protective effect against food allergy (OR = 0.95 (0.92–0.99)). A pro-inflammatory diet was linked to increased asthma/wheeze risk in children under 5 (OR = 1.17 (1.04, 1.33)) and (OR = 1.18 (1.04, 1.34)) with high heterogeneity across studies. Modest evidence supports a protective role of diet diversity against food allergy and that pro-inflammatory diets may increase early asthma risk in children. The Maternal diet index is the only index significantly associated with multiple allergy outcomes, and further studies in other cohorts are required.

Recent epidemiological studies have suggested a positive association between ultra-processed food consumption and breast cancer risk, although some studies also reported no association. Furthermore, the evidence regarding the associations between intake of food with lower degrees of processing and breast cancer risk is limited.

Thus, we investigated the associations between dietary intake by degree of food processing and breast cancer risk, overall and by breast cancer subtypes in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.

Dietary intake of EPIC participants was assessed via questionnaires at baseline. More than 11,000 food ingredients were classified into four groups of food processing levels using the NOVA classification system: unprocessed/minimally processed (NOVA 1), culinary ingredients (NOVA 2), processed (NOVA 3) and ultra-processed (NOVA 4). Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of breast cancer per standard deviation increase in daily consumption (grams) of foods from each NOVA group.

The current analysis included 14,933 breast cancer cases, diagnosed among the 318,686 EPIC female participants, (median follow-up of 14.9 years). No associations were found between breast cancer risk and the level of dietary intake from NOVA 1 [HR _{per 1 SD}=0.99 (95% CI 0.97 – 1.01)], NOVA 2 [HR _{per 1 SD} =1.01 (95% CI 0.98 – 1.03)] and NOVA 4 [HR _{per 1 SD} =1.01 (95% CI 0.99 – 1.03)] foods. However, a positive association was found between NOVA 3 and breast cancer risk [HR _{per 1 SD} =1.05 (95% CI 1.03 – 1.07)] which became non-significant after adjustment for alcohol intake [HR _{per 1 SD} =1.01 (95% CI 0.98 – 1.05)] or when beer and wine were excluded from this group [HR _{per 1 SD} =0.99 (95% CI 0.97 – 1.01)]. The associations did not differ by breast cancer subtype, menopausal status or body mass index. Findings from this large-scale prospective study suggest that the positive association between processed food intake and breast cancer risk was likely driven by alcoholic beverage consumption.

We investigated data-driven and hypothesis-driven dietary patterns and their association to plasma metabolite profiles and subsequent colorectal cancer (CRC) risk in 680 CRC cases and individually matched controls. Dietary patterns were identified from combined exploratory/confirmatory factor analysis. We assessed association to LC–MS metabolic profiles by random forest regression and to CRC risk by multivariable conditional logistic regression. Principal component analysis was used on metabolite features selected to reflect dietary exposures. Component scores were associated to CRC risk and dietary exposures using partial Spearman correlation. We identified 12 data-driven dietary patterns, of which a breakfast food pattern showed an inverse association with CRC risk (OR per standard deviation increase 0.89, 95% CI 0.80–1.00, p = 0.04). This pattern was also inversely associated with risk of distal colon cancer (0.75, 0.61–0.96, p = 0.01) and was more pronounced in women (0.69, 0.49–0.96, p = 0.03). Associations between meat, fast-food, fruit soup/rice patterns and CRC risk were modified by tumor location in women. Alcohol as well as fruit and vegetables associated with metabolite profiles (Q² 0.22 and 0.26, respectively). One metabolite reflecting alcohol intake associated with increased CRC risk, whereas three metabolites reflecting fiber, wholegrain, and fruit and vegetables associated with decreased CRC risk.

Background: Food biodiversity in human diets has potential co-benefits for both public health and sustainable food systems. However, current evidence on the potential relationship between food biodiversity and cancer risk, and particularly gastrointestinal cancers typically related to diet, remains limited. This study evaluated how dietary species richness (DSR) was associated with gastrointestinal cancer risk in a pan-European population.

Methods: Associations between DSR and subsequent gastrointestinal cancer risk were examined among 450,111 adults enrolled in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC, initiated in 1992), free of cancer at baseline. Usual dietary intakes were assessed at recruitment with country-specific dietary questionnaires. DSR of an individual's yearly diet was calculated based on the absolute number of unique biological species in each food and drink item. Associations between DSR and cancer risk were assessed by multivariable Cox proportional hazards regression models.

Findings: During a median follow-up time of 14.1 years (SD=3.9), 10,705 participants were diagnosed with gastrointestinal cancer. Hazard ratios (HRs) and 95 % confidence intervals (CIs) comparing overall gastrointestinal cancer risk in the highest versus lowest quintiles of DSR indicated inverse associations in multivariable-adjusted models [HR (95 % CI): 0.77 (0.69–0.87); P-value < 0·0001] (Table 2). Specifically, inverse associations were observed between DSR and oesophageal squamous cell carcinoma, proximal colon, colorectal, and liver cancer risk (p-trend<0.05 for all cancer types).

Interpretation: Greater food biodiversity in the diet may lower the risk of certain gastrointestinal cancers. Further research is needed to replicate these novel findings and to understand potential mechanisms.