Association of Repeated Antibiotic Exposure Up to Age 4 Years With Body Mass at Age 4.5 Years

Chelimo, Carol; Camargo, Carlos A.; Morton, Susan; Grant, Cameron

doi:10.1001/jamanetworkopen.2019.17577

Cited by 41 publications

(39 citation statements)

References 23 publications

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“…In sharp contrast to previous studies, only two studies have reported no difference between exposure to antibiotics and childhood overweight/obesity [ 112 , 118 , 119 ]. However, in the first study, only a single class of antibiotics was prescribed as prophylaxis; therefore, the results might have been affected by the type and dosage of the administered antibiotic, while in the second study, infection per se rather than the administration of antibiotics accounted for the observed increased body weight.…”

Section: Administration Of Antibiotics As a Cause Of Obesitycontrasting

confidence: 70%

“… ✓ Increased number of antibiotic classes, longer duration of antibiotic administration and earlier antibiotics administration (before 24 months of age) was related to childhood obesity at 30–36 months of age. Chelimo et al 2020[ 118 ] 6,853 children aged 54 months, New Zealand I) Antibiotics administration during 48 months of age ✓ Administration of antibiotics for ≥ 9 times was related to an increased likelihood of obesity, when compared with no exposure (adjusted odds ratio, 2.41; 95% CI, 1.07–5.41). Children whose exposure began in the 1 year of life had a higher adjusted mean (SD) BMI-for-age z score than those not exposed (1.06 [0.05] vs 0.89 [0.09]; P = .03), ✓ Repeated antibiotics administration in early childhood was related to a higher mean BMI-for-age z score and an increased likelihood of obesity.…”

Section: Administration Of Antibiotics As a Cause Of Obesitymentioning

confidence: 99%

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Do Antibiotics Cause Obesity Through Long-term Alterations in the Gut Microbiome? A Review of Current Evidence

et al. 2021

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Purpose of Review In this review, we summarize current evidence on the association between antibiotics and the subsequent development of obesity through modulation of the gut microbiome. Particular emphasis is given on (i) animal and human studies and their limitations; (ii) the reservoir of antibiotics in animal feed, emerging antibiotic resistance, gut dysbiosis, and obesity; (iii) the role of infections, specifically viral infections, as a cause of obesity; and (iv) the potential therapeutic approaches other than antibiotics to modulate gut microbiome. Recent Findings Overall, the majority of animal studies and meta-analyses of human studies on the association between antibiotics and subsequent development of obesity are suggestive of a link between exposure to antibiotics, particularly early exposure in life, and the development of subsequent obesity as a result of alterations in the diversity of gut microbiota. The evidence is strong in animal models whereas evidence in humans is inconclusive requiring well-designed, long-term longitudinal studies to examine this association. Based on recent meta-analyses and epidemiologic studies in healthy children, factors, such as the administration of antibiotics during the first 6 months of life, repeated exposure to antibiotics for ≥ 3 courses, treatment with broad-spectrum antibiotics, and male gender have been associated with increased odds of overweight/obesity. Early antibiotic exposure in animal models has shown that reductions in the population size of specific microbiota, such as Lactobacillus , Allobaculum , Rikenellaceae , and Candidatus Arthromitus , are related to subsequent adiposity. These data suggest that the loss of diversity of the gut microbiome, especially early in life, may have potential long-term detrimental effects on the adult host gut microbiome and metabolic health. Genetic, environmental, and age-related factors influence the gut microbiome throughout the lifetime. More large-scale, longer-term, longitudinal studies are needed to determine whether changes that occur in the microbiome after exposure to antibiotics, particularly early exposure, are causal of subsequent weight gain or consequent of weight gain in humans. Summary Further well-designed, large-scale RCTs in humans are required to evaluate the effects of administration of antibiotics, particularly early administration, and the subsequent development of overweight/obesity. Therapeutic interventions, such as bacteriophage treatment or the use of probiotics, especially genetically engineered ones, need to be evaluated in terms of prevention and management of obesity.

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Section: Administration Of Antibiotics As a Cause Of Obesitycontrasting

confidence: 70%

Section: Administration Of Antibiotics As a Cause Of Obesitymentioning

confidence: 99%

Do Antibiotics Cause Obesity Through Long-term Alterations in the Gut Microbiome? A Review of Current Evidence

et al. 2021

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“…The main limitation of this study is that potentially important covariates associated with the development of childhood obesity may have not been included in the final multivariate models and, thus, the magnitude of the association between the IFI and obesity may be overestimated. Examples of covariates include objective infant PA and sleep measures which were not measured in the preschool years in this cohort, mode of delivery and antibiotic use, both recently reported as associated with child body size in this cohort (53,54) . The exclusion of children born with low-birth weight and preterm aimed to accounr for children more likely to have medical and developmental issues that may impcat feeding and growth.…”

Section: Study Findings In Relation To Other Studiesmentioning

confidence: 99%

An index measuring adherence to New Zealand Infant Feeding Guidelines has convergent validity with maternal socio-demographic and health behaviours and with children’s body size

et al. 2021

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Using data from a nationally generalisable birth cohort, we aimed to: (i) describe the cohort’s adherence to national evidence-based dietary guidelines using an Infant Feeding Index (IFI) and (ii) assess the IFI’s convergent construct validity, by exploring associations with antenatal maternal socio-demographic and health behaviours and with child overweight/obesity and central adiposity at age 54 months. Data were from the Growing Up in New Zealand cohort (n 6343). The IFI scores ranged from zero to twelve points, with twelve representing full adherence to the guidelines. Overweight/obesity was defined by BMI-for-age (based on the WHO Growth Standards). Central adiposity was defined as waist-to-height ratio > 90th percentile. Associations were tested using multiple linear regression and Poisson regression with robust variance (risk ratios, 95 % CI). Mean IFI score was 8·2 (sd 2·1). Maternal characteristics explained 29·1 % of variation in the IFI score. Maternal age, education and smoking had the strongest independent relationships with IFI scores. Compared with children in the highest IFI tertile, girls in the lowest and middle tertiles were more likely to be overweight/obese (1·46, 1·03, 2·06 and 1·56, 1·09, 2·23, respectively) and boys in the lowest tertile were more likely to have central adiposity (1·53, 1·02, 2·30) at age 54 months. Most infants fell short of meeting national Infant Feeding Guidelines. The associations between IFI score and maternal characteristics, and children’s overweight/obesity/central adiposity, were in the expected directions and confirm the IFI’s convergent construct validity.

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“…However, this process is vulnerable and can be disturbed by various pre‐, intra‐, and post‐partum factors, including delivery and feeding modes, antibiotics, maternal overweight and diet, and gestational diabetes 131 . Interestingly, all these factors are linked to increased susceptibility to adolescent and (or) adult obesity 132–137 . A large‐scale longitudinal birth cohort study indicated that early‐life infection, rather than antibiotic administration, is associated with late‐life obesity, 138 which indicates that inflammatory responses, as seen during early‐life gut dysbiosis, increases the susceptibility to obesity.…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

“…131 Interestingly, all these factors are linked to increased susceptibility to adolescent and (or) adult obesity. [132][133][134][135][136][137] A large-scale longitudinal birth cohort study indicated that early-life infection, rather than antibiotic administration, is associated with late-life obesity, 138 which indicates that inflammatory responses, as seen during early-life gut dysbiosis, increases the susceptibility to obesity.…”

Section: Correlations Between Serum Iga and Metsmentioning

confidence: 99%

Interaction between IgA and gut microbiota and its role in controlling metabolic syndrome

et al. 2020

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Summary Immunoglobulin A (IgA) is the most abundant immunoglobulin isotype secreted into the mucosal tissues, mainly intestinal mucus. Humans can produce several grams of IgA every day, accounting for three quarters of the body's total immunoglobulin content. IgA, together with mucus and antimicrobial peptides, forms the first line of defence for intestinal epithelial cells, protecting them from a significant number of intestinal antigens. IgA also plays a principal role in controlling the gut microbiota (GM), and disruption in IgA can result in dysbiosis, such as the enrichment of Proteobacteria, which are generally bound by IgA. Proteobacteria overexpansion is also usually seen in obesity and colitis. Consistent with this, IgA dysfunction frequently results in metabolic syndrome (MetS), including conditions such as obesity, adiposity, insulin resistance, and inflammation. In contrast, enhanced IgA function can improve, and even prevent, MetS. Interactions among IgA, GM, and metabolism provide a promising avenue to combat MetS.

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Association of Repeated Antibiotic Exposure Up to Age 4 Years With Body Mass at Age 4.5 Years

Cited by 41 publications

References 23 publications

Do Antibiotics Cause Obesity Through Long-term Alterations in the Gut Microbiome? A Review of Current Evidence

Do Antibiotics Cause Obesity Through Long-term Alterations in the Gut Microbiome? A Review of Current Evidence

An index measuring adherence to New Zealand Infant Feeding Guidelines has convergent validity with maternal socio-demographic and health behaviours and with children’s body size

Interaction between IgA and gut microbiota and its role in controlling metabolic syndrome

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