Background The evidence on the relationship between diet diversity in early life and allergic outcomes was few and inconsistent. We sought to determine the association of food diversity in the first year of life with allergic outcomes in the second year. Methods Two thousand two hundred fifty‐one mother‐infant pairs from Tongji Maternal and Child Health Cohort (TMCHC) were involved in the study. Information on complementary foods introduction was obtained by telephone interview at 6‐ and 12‐month postpartum follow‐up. Any doctor‐diagnosed allergic diseases in the second year were recorded at 2‐year postpartum follow‐up. Food allergies in infancy were assessed and self‐reported by mothers at each postpartum follow‐up. Multivariable logistic regression was used to examine the effect of food diversity at 6 and 12 months of age on later allergic diseases and food allergy. Results A total of 135 (6.0%) infants reported allergic diseases at between 1 and 2 years of age. Independent of food allergy history of infants and other potential confounders, less food diversity at 6 months of age was associated with increased risk of later allergic diseases (OR 2.17, 95% CI 1.04–4.50 for 0 vs. 3–6 food groups). By 12 months of age, significant inverse associations with later allergic diseases (OR 2.35, 95% CI 1.03–5.32 for 1–5 vs. 8–11 food groups, and OR 1.98, 95% CI 1.16–3.37 for 6–7 vs. 8–11 food groups) and food allergy (OR 2.10, 95% CI 1.29–3.42 for 1–5 vs. 8–11 food groups) were observed. Children with higher food diversity in both periods had the lowest risk of allergic diseases during the second year of life. Conclusions A more diverse diet within the first year of life was associated with reduced risk of allergic diseases at 1–2 years of age. Introducing higher diversity of foods from 6 to 12 months of age might be an effective strategy to improve the allergy outcomes of infants in later life.

Background Osteoarthritis (OA) is a worldwide public health concern, mainly afflicting older adults. Although the etiology of OA remains unclear, environmental factors are increasingly considered as non-negligible risk factors. This study aims to evaluate the associations of urinary metals with OA risk and the mediated effect of biological aging. Methods Nine urinary metal concentrations were detected among 12,584 U.S. adults based on the National Health and Nutrition Examination Survey (NHANES), including barium (Ba), cadmium (Cd), cobalt (Co), cesium (Cs), molybdenum (Mo), lead (Pb), antimony (Sb), thallium (Tl), and uranium (Tu). Multivariable logistic regression and weighted quantile sum (WQS) regression were used to explore the associations of single metal and mixed metals with OA risk, respectively. Furthermore, biological aging was measured from different perspectives, including cell senescence (telomere length) and whole-body aging (phenotypic age and biological age). Mediation analyses were conducted to investigate the mediated effects of aging on the associations of metals with OA risk. Results In the single-exposure model, Cd, Co, and Cs were identified to be positively associated with OA risk, with odds ratios (OR) ranging from 1.48 to 1.64 (all P < 0.05). Mixed-exposure analyses showed consistent associations (OR 1.23, 95%CI 1.10 to 1.37) and highlighted that Cd, Co, and Cs were responsible for the outcomes. Additionally, Cd, Co, Cs, Pb, and Tl were positively associated with biological aging markers, while all biological aging markers had significant associations with OA risk. Further mediation analyses showed that the associations of single metal (mainly Cd and Cs) and mixed metals with OA risk parallelly mediated by the above biological aging markers, with the proportion of mediation ranging from 16.89 to 69.39% (all P < 0.05). Moreover, such associations were also serially mediated through telomere length-biological age path and telomere length-phenotypic age path (the proportion of mediation: 4.17–11.67%), indicating that metals accelerated cell senescence to lead to whole-body aging and finally aggravated OA progress. Conclusions These findings suggested that exposure to metals increased OA risk, which was possibly and partly mediated by biological aging.

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