Infectious disease is a leading cause of morbidity and hospitalization for infants and children. During infancy, breast-feeding protects against infectious diseases, particularly respiratory infections, gastrointestinal infections, and otitis media. Little is known about the longer-term impact of breast-feeding on infectious disease in children. We investigated the relationship between infant feeding and childhood hospitalizations from respiratory and gastrointestinal infections in a population-based birth cohort of 8327 children born in 1997 and followed for 8 years. The main outcomes were public hospital admissions for respiratory infections, gastrointestinal infections, and all infectious diseases. Cox regression was used to assess time to first hospitalization. Breast-feeding only (no formula-feeding) for 3 or more months was associated with a lower risk of hospital admission in the first 6 months of life for respiratory infections (hazard ratio = 0.64 [95% confidence interval = 0.42–0.97]), gastrointestinal infections (0.51 [0.25–1.05]), and any infection (0.61 [0.44–0.85]), adjusted for sex, type of hospital at birth, and household income. Partial breast-feeding (both breast-feeding and formula-feeding) in the first 3 months also reduced hospitalizations from infections but with smaller effect sizes. Beyond 6 months of age, there was no association between breast-feeding status at 3 months and hospitalization for infectious disease. Giving breast milk and no formula for at least 3 months substantially reduced hospital admissions for many infectious diseases in the first 6 months of life, when children are most vulnerable.

This study aims to evaluate the causal association of blood pressure (BP) with cardiovascular diseases (CVDs). Two-sample Mendelian randomization was performed using a large genome-wide association study (n=299 024) and the UK Biobank cohort (n=375 256). We identified 327 and 364 single-nucleotide polymorphisms strongly and independently associated with systolic BP and diastolic BP, respectively, as genetic instruments to assess the causal association of BP with total CVD, CVD mortality, and 14 cardiovascular conditions. Nonlinearity was examined with nonlinear instrumental variable assumptions. Genetically predicted BP was significantly positively associated with total CVD (systolic BP, per 10 mm Hg: odds ratio [OR], 1.32 [95% CI, 1.25–1.40]; diastolic BP, per 5 mm Hg: OR, 1.20 [95% CI, 1.15–1.26]). Similar positive causal associations were observed for 14 cardiovascular conditions including ischemic heart disease (systolic BP, per 10 mm Hg: OR, 1.33 [95% CI, 1.24–1.41]; diastolic BP, per 5 mm Hg: OR, 1.20 [95% CI, 1.14–1.27]) and stroke (systolic BP, per 10 mm Hg: OR, 1.35 [95% CI, 1.24–1.48]; diastolic BP, per 5 mm Hg: OR, 1.20 [95% CI, 1.12–1.28]). Nonlinearity Mendelian randomization test demonstrated linear causal association of BP with these outcomes. Consistent estimates were observed in sensitivity analyses, suggesting robustness of the associations and minimal horizontal pleiotropy. The linear positive causal association of BP and CVD was consistent with previous findings that lower BP is better, thus consolidating clinical knowledge on hypertension management in CVD risk reduction.

Manipulation of the gut microbiota presents a new opportunity to combat chronic diseases. Randomized controlled trials of probiotics suggest some associations with adiposity, lipids, and insulin resistance, but to our knowledge no trials with “hard” outcomes have been conducted. We used separate-sample Mendelian randomization to obtain estimates of the associations of 27 genera of gut microbiota with ischemic heart disease, type 2 diabetes mellitus, adiposity, lipid levels, and insulin resistance, based on summary data from CARDIoGRAAMplusC4D and other consortia. Among the 27 genera, a 1-allele increase in single nucleotide polymorphisms related to greater abundance of Bifidobacterium was associated with lower risk of ischemic heart disease (odds ratio = 0.985, 95% confidence interval (CI): 0.971, 1.000; P = 0.04), a 0.011–standard-deviation lower body mass index (95% CI: −0.017, −0.005), and a 0.026–standard-deviation higher low-density lipoprotein cholesterol level (95% CI: 0.019, 0.033), but the findings were not robust to exclusion of potential pleiotropy. We also identified Acidaminococcus, Aggregatibacter, Anaerostipes, Blautia, Desulfovibrio, Dorea, and Faecalibacterium as being nominally associated with type 2 diabetes mellitus or other risk factors. Results from our study indicate that these 8 genera of gut microbiota should be given priority in future research relating the gut microbiome to ischemic heart disease and its risk factors.

Background Observational studies from mainly Western settings suggest breastfeeding may protect against childhood adiposity; however, breastfeeding and adiposity share social patterning potentially generating confounding, making evidence from other settings valuable. Methods We used multivariable linear regression to examine the prospective adjusted associations of breastfeeding with body mass index (BMI), height and weight z-scores at 7 years of age relative to the 2007 World Health Organization (WHO) growth reference, in a large (n = 8327), population-representative Hong Kong Chinese birth cohort, recruited between April and May 1997 with high follow-up (n = 7026). Results Low socio-economic position (SEP) was associated with never breastfeeding and with exclusive breastfeeding for ≥3 months. We did not find any association between breastfeeding and BMI [z-score mean difference 0.07, 95% confidence interval (CI) –0.05 to 0.19], height (0.02, 95% CI –0.07 to 0.11) or weight (0.07, 95% CI –0.05 to 0.18), adjusted for sex, birth weight, gestational age, SEP, second-hand smoke (SHS) exposure, parity, mother's age at birth, mother's place of birth and serious infant morbidity. Conclusions In a non-European setting, breastfeeding was not associated with child adiposity, suggesting that observed protective effects may be due to socially patterned confounding by SEP, maternal adiposity and maternal smoking.

Early-life air pollution exposure is associated with lung function in children and adolescents. However, whether the association of prenatal and early postnatal exposure to air pollution with lung function continues into adulthood remains unclear. To investigate the associations of early exposure to air pollution with lung function at ~17.5 years in a non-western developed setting with more concentrated air pollutants. We examined the associations of exposure to particular matter with an aerodynamic diameter of <10 μm (PM10), nitrogen dioxides (NO2), nitric oxide (NO), sulfur dioxide (SO2) in standard deviations (SD)) at different early life stages with lung function (indicated by forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25%-75% of the pulmonary volume (FEF25%-75%)) in SD at ~17.5 years, personal history of wheezing and asthma in the population-representative Hong Kong Chinese birth cohort "Children of 1997"(n = 2942). Higher in utero and infancy and toddlerhood NO2 were associated with lower FEV1 (-0.022, 95% confidence interval (CI) -0.029 to -0.015 and - 0.026, 95% CI -0.033 to -0.019), FEV1/FVC (-0.035, 95% CI -0.050 to -0.021 and -0.052, 95% CI -0.066 to -0.038) and FEF25%-75% (-0.031, 95% CI -0.040 to -0.022 and -0.043, 95% CI -0.051 to -0.035). A similar association was observed for NO. Weak associations of NO2 and NO with FVC were observed (-0.011, 95% CI -0.018 to -0.003 and -0.010, 95% CI -0.020 to -0.001). NOx was associated with higher risk of wheezing (1.08, 95% CI 1.03 to 1.14) but not asthma (1.02, 95% CI 0.94 to 1.11). SO2 and PM10 were not clearly associated with lung function, wheezing or asthma. Our findings suggest that early exposure to air pollution from NO2 may have long-term effects on lung function, which could affect respiratory health throughout life.

Observationally, coffee is inversely associated with type 2 diabetes mellitus (T2DM), depression and Alzheimer’s disease, but not ischemic heart disease (IHD). Coffee features as possibly protective in the 2015 Dietary Guidelines for Americans. Short-term trials suggest coffee has neutral effect on most glycemic traits, but raises lipids and adiponectin. To clarify we compared T2DM, depression, Alzheimer’s disease, and IHD and its risk factors by genetically predicted coffee consumption using two-sample Mendelian randomization applied to large extensively genotyped case-control and cross-sectional studies. Childhood cognition was used as a negative control outcome. Genetically predicted coffee consumption was not associated with T2DM (odds ratio (OR) 1.02, 95% confidence interval (CI) 0.76 to 1.36), depression (0.89, 95% CI 0.66 to 1.21), Alzheimer’s disease (1.17, 95% CI 0.96 to 1.43), IHD (0.96, 95% CI 0.80 to 1.14), lipids, glycemic traits, adiposity or adiponectin. Coffee was unrelated to childhood cognition. Consistent with observational studies, coffee was unrelated to IHD, and, as expected, childhood cognition. However, contrary to observational findings, coffee may not have beneficial effects on T2DM, depression or Alzheimer’s disease. These findings clarify the role of coffee with relevance to dietary guidelines and suggest interventions to prevent these complex chronic diseases should be sought elsewhere.