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Antibiotic treatment during infancy and increased body mass index in boys: an international cross-sectional study



To investigate whether antibiotic exposure during the first year of life is associated with increased childhood body mass index (BMI).


Secondary analysis from a multi-centre, multi-country, cross-sectional study (The International Study of Asthma and Allergies in Childhood Phase Three).


A total of 74 946 children from 31 centres in 18 countries contributed data on antibiotic use in the first 12 months of life and current BMI.


Parents/guardians of children aged 5–8 years completed questionnaires that included questions about their children’s current height and weight, and whether in the child’s first 12 months of life, they had received any antibiotics, paracetamol, were breastfed or the mother/female guardian smoked cigarettes, and whether the child had wheezed in the past 12 months. A general linear mixed model was used to determine the association of antibiotic exposure with BMI, adjusting for age, sex, centre, BMI measurement type (self-reported or measured), maternal smoking, breastfeeding, paracetamol use, gross national income and current wheeze.


There was a significant interaction between sex and early-life antibiotic exposure. Early-life antibiotic exposure was associated with increased childhood BMI in boys (+0.107 kg m−2, P<0.0001), but not in girls (−0.008 kg m−2, P=0.75) after controlling for age, centre and BMI measurement type. The association remained in boys (+0.104 kg m−2, P<0.0007), after adjustment for maternal smoking, breastfeeding, paracetamol use and current wheeze. There was no interaction between age, maternal smoking, breastfeeding, paracetamol use, gross national income and current wheeze in the association between early antibiotic exposure and BMI.


Exposure to antibiotics during the first 12 months of life is associated with a small increase in BMI in boys aged 5–8 years in this large international cross-sectional survey. By inference this provides additional support for the importance of gut microbiota in modulating the risk of obesity, with a sex-specific effect.


The increasing prevalence of overweight and obesity in both children and adults is an international health concern1 owing to the association with increased morbidity, mortality and health-care costs.2 Obesity results from a combination of genetic3 and environmental factors4 that promote excess energy intake and reduced energy expenditure. The gut is colonised by a large number of organisms that are collectively known as microbiota. Recent evidence suggests that gut microbiota composition and function have a major role in the digestion and energy conversion of nutrients ingested and may be involved in the pathogenesis of obesity.5, 6 Early life appears to be a critical period for normal gut microbiota colonisation, which can be interrupted by antibiotic administration.7 Recent reports suggest that exposure to antibiotics in early life may be linked to subsequent obesity in animals8 and children.9, 10

Many different classes of antibiotics have long been been used to promote weight gain in farm animals.11, 12 Antibiotics, particularly when administered early in life, are known to affect gut microbiota colonisation and increase the efficiency of animal-feeding practice with greatest weight gain occurring with earlier antibiotic use.13 Recent studies show that mice treated with antibiotics early in life gain more weight and accumulate more fat due to altered gut microbiota, which shift their digestion towards greater energy extraction and reduced residual energy in the faeces.8

An association between early antibiotic exposure and subsequent increased body mass of children has been reported in two European studies conducted among the Danish National Birth Cohort10 and the Avon Longitudinal Study of Parents and Children.9 Antibiotics have recently been shown to be an effective adjunctive therapy in the management of severe, acute malnutrition in the form of kwashiorkor,14 a condition that has been shown to be linked with altered gut microbiota.15 Given that gut microbiota diversity, types and function is reported to be different in rural African children with lower obesity prevalence compared with contemporary European children,16 the association of early antibiotic use and childhood body mass index (BMI) in different populations is worth investigating.

We examined whether antibiotic exposure within the first year of life was associated with increased BMI of 5–8-year-old children participating in the large, International Study of Asthma and Allergies in Childhood (ISAAC). We took into account several factors that may confound this association by being related both to the propensity for early-life antibiotic use and subsequent BMI: maternal smoking during the first year of life and breastfeeding (both variably reported to be associated with offspring BMI) that may also affect early-life antibiotic use through altering susceptibility to respiratory infections;17, 18 current wheeze (a marker of asthma that is both associated with increased BMI and may have caused respiratory symptoms in early life that may have led to increased antibiotic use19). Given that dietary and other exposures related to the economic status of a country may influence gut microbiota, we examined whether gross national income affected any association between early antibiotic exposure and subsequent BMI. In addition, we included paracetamol use in the first year of life, as a test of spurious association of early-life medication use unrelated to gut microbiota alterations and which may reflect unmeasured parental lifestyle confounders associated with receptivity to administration of medication in children.


The ISAAC study is a multi-centre, multi-country, multi-phase, cross-sectional study investigating the prevalence of the symptoms of asthma, rhinoconjuctivitis and eczema and the role of risk factors and has previously been described.20 ISAAC Phase Three was undertaken from 2000–2003 and involved 5–8-year-old children chosen from a random sample of schools in defined geographical areas. It used the Phase One standardised Core Questionnaire on symptoms of asthma, rhinoconjunctivitis and eczema and included an optional environmental questionnaire to collect specific aetiological data including height, weight, antibiotic use and parental smoking. Parents or guardians completed questionnaires for those aged 5–8 years. The questionnaires were translated from English into the local language and then back-translated into English for verification.21 The following questions were used to ascertain antibiotic use, breastfeeding, maternal smoking status, current asthma symptoms and paracetamol use: in the first 12 months of life, did your child have any antibiotics? Was your child breastfed? Did your child’s mother (or female guardian) smoke cigarettes during your child’s first year of life? In the first 12 months of your child’s life, did you usually give paracetamol (for example, Panadol and Pamol) for fever? Has your child had wheezing or whistling in the chest in the past 12 months? All responses were categorised as yes or no. The questionnaires are available on the ISAAC website

Childrens’ height and weight were reported by parents, and in some centres height and weight were measured objectively (although there were no standardised or specific instructions for doing this). To eliminate likely erroneous data, those children in the top and bottom 0.5% of weights and heights for each centre, and those with heights less than 1.0 metre were excluded. BMI was calculated (weight (kg)/height (m)2) and all BMIs less than 9 kg m−2 and greater than 40 kg m−2 were removed (see Figure 1). To be included in the analysis, centres had to have at least 70% complete BMI data and 70% complete antibiotic data. Individuals without complete age, sex, BMI and antibiotic data were excluded (see Figure 1).

Figure 1

Flowchart of the study population of 5–8-year-old children.

Statistical analysis

The association between antibiotic exposure in the first year of life and individual childhood BMI was assessed using a general linear mixed model with sex within centre as the random effect, and fixed effects of age, sex, BMI measurement type (by parent report or using objective measurement of height and weight) and early antibiotic use. Further analyses were done including maternal smoking, breastfeeding, current wheeze and early-life paracetamol use in the model. The interaction of early-life antibiotic exposure with age, exposure to maternal smoking, breastfeeding, current asthma symptoms and paracetamol administration (in the first 12 months of life) was examined. We tested for interactions with gross national income of each country according to the World Bank data by categorising countries as having low income or higher (lower middle, upper middle or high) income (non-affluent or affluent).22 Analyses used SAS (v 9.2, SAS Institute, Cary, NC, USA).


A total of 74 946 children from 31 centres in 18 countries contributed data on both BMI and antibiotic use in the first 12 months of life and were included in the final analysis (see Figure 1). Of these, measured height and weight data were available on 15 253 subjects from seven centres in seven countries and the remainder were parent-reported height and weight data. The prevalence of antibiotic use in the first year of life ranged from 76% in Thailand to 22% in Taiwan (Figure 2). The frequency of maternal smoking in the first year of life ranged from 0–35% (median 12%), breastfeeding 27–98% (median 77%), paracetamol use in the first year of life 10–87% (median 61%), current wheeze 3–22% (median 8%). Five of the 18 countries were classified as non-affluent that is, Nigeria, India, Indonesia, Thailand and Syria.

Figure 2

Association between antibiotic use in the first year of life and childhood BMI by centres in different countries. The difference in BMI (kg m−2) between 5–8-year-old (a) boys and (b) girls exposed to antibiotics in the first year of life compared with those who were not, in each country by centre. For each country, the proportion of children who were exposed to antibiotics in the first year of life is shown in parentheses. Those centres with parent-reported heights and weights are shown with filled circles, and those centres that measured heights and weights are shown with hollowed circles. Overlapping circles are displayed vertically. The diamond labelled ‘overall’ gives the estimate and 95% confidence limits for all the points above.

There was a significant interaction between sex and antibiotic exposure during the first 12 months of life and subsequent childhood BMI (P=0.002) in the model that controlled for age, centre and BMI measurement type (self-reported or measured). An association between early-life antibiotic use and BMI at the age of 5–8 years was observed in boys (+0.107 kg m−2, P<0.0001), but not in girls (−0.008 kg m−2, P=0.75). This effect and sex interaction remained in the subset with measured height and weight data.

In sex-specific models examining the regression of BMI with antibiotic exposure controlling for age, measurement type, maternal smoking, breastfeeding, current wheezing, early-life paracetamol use and gross national income, the interaction terms of these variables with antibiotics were not statistically significant and were removed from the model. After additional adjustment for these additional variables, the association between early antibiotic use and childhood BMI remained statistically significant among boys (+0.104 kg m−2, P<0.0007), but not in girls (−0.028 kg m−2, P=0.34). The difference in BMI between boys and girls with or without antibiotic exposure in the first year of life is shown for each centre within the country in boys (Figure 2a) and girls (Figure 2b).


This large, international population-based cross-sectional study examining 74 946 children confirms that early-life antibiotic exposure (in the first 12 months of life) is associated with a significant increase in BMI (+0.107 kg m−2, P<0.0001) among boys but not girls aged between 5 and 8 years. The relationship of early antibiotic use with increased BMI was not explained by any interaction with age within the 5–8 year range, maternal smoking in the first year of life, breastfeeding, current wheeze or early-life paracetamol administration. The prevalence of antibiotic exposure varied greatly between the different participating countries ranging from 76% in Thailand to 22% in Taiwan.

Two previous human studies have reported an association between early-life antibiotic use and subsequent increased childhood body mass. A study of 28 354 children from Denmark reported an increased risk of overweight at 7 years after antibiotic administration in the first 6 months of life among those born to normal weight mothers, which was not seen among those born to overweight or obese mothers.10 We did not have data on maternal BMI to investigate this interaction. A study of 11 532 children born in the United Kingdom, reported that antibiotic use in the first 6 months of life was associated with increased weight for length at 10 months (+0.10 s.d. scores), 20 months (+0.08 s.d. scores) and BMI at 38 months (+0.07 kg m−2), but not at 7 years of age.8 This UK study showed no association of antibiotic exposure between 6–14 months and subsequent BMI, however, those who received antibiotics in the 15–23-month window had elevated BMI (Z-score of +0.05 s.d. units) at 7 years. In contrast, our results show a consistent effect of antibiotic exposure in the first 12 months of life and increased BMI (+0.107 kg m−2) between the age of 5–8 years among boys only. Addition of gross national income to our model made no difference to the antibiotic regression coefficient and there was no interaction between country affluence and antibiotic exposure, suggesting that these effects were not dependent on other factors associated with economic development.

Sex differences in reporting bias of body measurement is unlikely to be the explanation behind the sex interaction we observed because the result was unchanged when we considered only those with measured values for height and weight. The susceptibility of male sex to the growth-promoting effects of antibiotics has been reported in two earlier human studies. In the Danish study, after adjustment for confounders, the increased risk of overweight with early antibiotic exposure only persisted among boys (odds ratio 1.75, 95% confidence interval 1.18–2.60) but not in girls, born to normal weight mothers.10 Male sex was also an independent predictor of increase in BMI (+1.1 kg m−2, P=0.02) following a 6-week vancomycin treatment of infective endocarditis in 48 adults compared with 48 age-matched controls.23 Animal studies of growth-promoting antibiotics have been associated with thinning of the gastrointestinal tract, and male chickens have been reported to have thinner and lighter weight tracts than females, likely contributing to more rapid growth observed in male chickens through improved nutrient absorption.24 Our finding of the BMI-promoting effects of antibiotics being confined to boys might be explained by sex-specific differences in intestinal adaptation to early-life antibiotic exposure or to how antibiotic drugs are metabolised.

The mechanisms by which antibiotics may increase body weight is likely to be multifactorial. In addition to promoting more effective nutrient absorption by causing a thinner intestinal epithelium, antibiotics may alter gut bacterial composition or function such that they have enhanced enzymatic activity to promote energy absorption, eliminate bacteria responsible for subclinical infections and reduce competing gut bacteria to allow more nutrient sparing for the host.8, 25 The functional consequences of antibiotic treatment on gut microbiota are only just beginning to be characterised and indicate a propensity for higher sugar anabolic capacities.26 The infant’s gut begins to be colonised in utero27 and during delivery, after which it progresses to dense colonisation until the age of 4 years when it resembles adult gut microbiota.28 In addition to antibiotic exposure,29 there is a likely contribution of host genetics,30 mode of delivery,31 breastfeeding32 and diet16 on the composition of stable adult microbiota. Given the likely differences in all these factors as well as hygiene, geography and climate in the participants of our large international study, our findings confirm the independent effect of early-life antibiotic use in promoting increased childhood BMI among boys.

There are several limitations to our study. First, exposure to antibiotics was measured by parental recall. Although memory of events that occurred up to 8 years previously could be imprecise, it is unlikely that recall of early antibiotic exposure would be associated with childhood BMI. Second, we did not collect data on antibiotic type, duration, mode of administration nor age of infant under 12 months when given. Each of these factors may potentially have differential impacts on gut microbiota and subsequent weight gain. The type of antibiotic used may be important, given that an association with adult obesity after intravenous vancomycin but not amoxycillin has been reported.23 A shorter duration and topical mode of administration (for example, antibacterial eye ointments), are less likely to affect gut microbiota compared with intravenous antibiotics based on their low systemic absorption.33 Antibiotics administered during the first 6 months of life, but not when given in the second 6 months of life were associated with increased childhood BMI in a previous study.9 Third, the relationship between antibiotic exposure and BMI is potentially confounded by many factors that we were not able to consider beyond maternal smoking, breastfeeding, wheezing and early-life paracetamol administration. Hence, it is difficult to disentangle the effect of the antibiotics from the effect of the condition that necessitated the use of antibiotics other than respiratory. Fourth, it was not possible to determine whether or not the temporal association observed was causal. Finally, the measurement type of BMI included either parent-reported or measured BMI. It is likely that weight may be inaccurately reported, but these inaccuracies are likely to have reduced any effect towards the null hypothesis, and thus our results may be a more conservative estimate of the effect of early antibiotic exposure. When we restricted our analysis to the subgroup in which measured data was used, our results were unchanged and remained significant in boys only. Nonetheless, this is the largest study reported to date, including children from many different ethnicities and likely different background lifestyle factors, showing a small but significant association with early-life antibiotic exposure and increased childhood BMI in boys between 5 and 8 years of age.

In conclusion, this largest study to date, confirms the association of early-life antibiotic exposure with increased BMI, only among boys from many different countries worldwide, which persists at least to 8 years of age. Further studies are required to identify whether these effects remain later in life, why boys are more susceptible and conversely, whether different antibiotics confer a different risk for BMI gain.


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EA Mitchell and I Braithwaite are supported in part by Cure Kids. The authors would like to thank ISAAC Phase Three Principal Investigators and Regional and National Coordinators as listed.

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Correspondence to R Murphy.

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The authors declare no conflict of interest.



ISAAC Steering Committee: N Aït-Khaled* (International Union Against Tuberculosis and Lung Diseases, Paris, France); HR Anderson (Division of Community Health Sciences, St Georges, University of London, London, UK); MI Asher (Department of Paediatrics: Child and Youth Health, Faculty of Medical and Health Sciences, The University of Auckland, New Zealand); R Beasley* (Medical Research Institute of New Zealand, Wellington, New Zealand); B Björkstén* (Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden); B Brunekreef (Institute of Risk Assessment Science, Universiteit Utrecht, Netherlands); J Crane (Wellington Asthma Research Group, Wellington School of Medicine, New Zealand); P Ellwood (Department of Paediatrics: Child and Youth Health, Faculty of Medical and Health Sciences, The University of Auckland, New Zealand); C Flohr (Department of Paediatric Allergy and Dermatology, St Johns Institute of Dermatology, St Thomas’ Hospital, London, UK); S Foliaki* (Centre for Public Health Research, Massey University, Wellington, New Zealand); F Forastiere (Department of Epidemiology, Local Health authority Rome, Italy); L García-Marcos (Respiratory Medicine and Allergy Units,‘Virgen de la Arrixaca’ University Children’s Hospital, University of Murcia, Spain); U Keil* (Institut für Epidemiologie und Sozialmedizin, Universität Münster, Germany); CKW Lai* (Department of Medicine and Therapeutics, The Chinese University of Hong Kong, SAR China); J Mallol* (Department of Paediatric Respiratory Medicine, University of Santiago de Chile, Chile); EA Mitchell (Department of Paediatrics: Child and Youth Health, Faculty of Medical and Health Sciences, The University of Auckland, New Zealand); S Montefort* (Department of Medicine, University of Malta, Malta), J Odhiambo* (Centre Respiratory Diseases Research Unit, Kenya Medical Research Institute, Nairobi, Kenya); N Pearce (Department of Medical Statistics, Faculty Epidemiology and Public Health, London School of Hygiene and Tropical Medicine, London, UK); CF Robertson (Murdoch Children’s Research Institute, Melbourne, Australia); AW Stewart (Population Health, Faculty of Medical and Health Sciences, The University of Auckland, New Zealand); D Strachan (Division of Community Health Sciences, St Georges, University of London, London, UK); E von Mutius (Dr von Haunerschen Kinderklinik de Universität München, Germany); SK Weiland† (Institute of Epidemiology, University of Ulm, Germany); G Weinmayr (Institute of Epidemiology, University of Ulm, Germany); H Williams (Centre for Evidence Based Dermatology, Queen’s Medical Centre, University Hospital, Nottingham, UK); G Wong (Department of Paediatrics, Prince of Wales Hospital, Hong Kong, SAR China). *Regional Coordinators; †Deceased.

ISAAC International Data Centre: MI Asher, TO Clayton, E Ellwood, P Ellwood, EA Mitchell, Department of Paediatrics: Child and Youth Health, and AW Stewart, School of Population Health, Faculty of Medical and Health Sciences, The University of Auckland, New Zealand.

ISAAC Principal Investigators: Belgium: J Weyler (Antwerp); Estonia: M-A Riikjärv* (Tallinn); Hungary: G Zsigmond* (Svábhegy); India: SN Mantri (Mumbai (29)); Indonesia: CB Kartasasmita (Bandung); Japan: H Odajima (Fukuoka); Lithuania: J Kudzyte* (Kaunas); Mexico: M Barragán-Meijueiro (Ciudad de México (3)), BE Del-Río-Navarro (Ciudad de México (1)), FJ Linares-Zapién (Toluca); Nigeria: BO Onadeko (Ibadan); Poland: A Brêborowicz (Poznan), G Lis* (Kraków); Portugal: C Nunes (Portimao); South Korea: H-B Lee* (Provincial Korea, Seoul); Spain: RM Busquets (Barcelona), I Carvajal-Urueña (Asturias), G García-Hernández (Madrid), L García-Marcos* (Cartagena), C González Díaz (Bilbao), A López-Silvarrey Varela (A Coruña), MM Morales-Suárez-Varela (Valencia); Sultanate of Oman: O Al-Rawas* (Al-Khod); Syrian Arab Republic: S Mohammad* (Tartous); Y Mohammad (Lattakia); Taiwan: J-L Huang* (Taipei); C-C Kao (Taoyuan); Thailand: M Trakultivakorn (Chiang Mai); P Vichyanond (Bangkok)*; Uruguay: MC Lapides (Paysandú). *National Coordinator.

ISAAC Phase Three National Coordinators not identified above: India: J Shah; Indonesia: K Baratawidjaja; Japan: S Nishima; Mexico: M Baeza-Bacab; Portugal: JE Rosado Pinto; Uruguay: D Holgado.

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Murphy, R., Stewart, A., Braithwaite, I. et al. Antibiotic treatment during infancy and increased body mass index in boys: an international cross-sectional study. Int J Obes 38, 1115–1119 (2014).

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  • antibiotic
  • gut microbiota
  • asthma
  • body mass index
  • overweight

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