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Early life nutrition and the opportunity to influence long-term health: an Australasian perspective

Part of: DOHaD ANZ Conference 2015

Published online by Cambridge University Press:  26 January 2016

P. S. W. Davies ,
J. Funder ,
D. J. Palmer ,
J. Sinn ,
M. H. Vickers ,
C. R. Wall  and
as the Australia and New Zealand Early Life Nutrition Working Party
P. S. W. Davies*
Affiliation:
School of Medicine, Children’s Nutrition Research Centre, University of Queensland, Herston, Queensland, Australia
J. Funder
Affiliation:
The Hudson Institute of Medical Research, Clayton, Victoria, Australia
D. J. Palmer
Affiliation:
School of Paediatrics and Child Health, University of Western Australia, Perth, Australia
J. Sinn
Affiliation:
Department of Obstetric and Gynaecology and Neonatology, University of Sydney, Australia
M. H. Vickers
Affiliation:
Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand
C. R. Wall
Affiliation:
Discipline of Nutrition and Dietetics, University of Auckland, New Zealand
*
*Address for correspondence: P. S.W. Davies, School of Medicine, Children’s Nutrition Research Centre, University of Queensland, Herston, QLD, Australia. (Email ps.davies@uq.edu.au)
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Abstract

There are now significant data to support the hypothesis that early life nutrition in the fetus, infant and young child can have profound effects on long-term health. This review considers some of this evidence with specific reference to the current burden of disease in Australia and New Zealand. As the findings of further research become available, recommendations on optimizing early life nutrition should be formulated and made widely available as part of the preventative health policy agenda in both Australia and New Zealand.

Keywords

early life nutritionhealthoutcomes

Information

Type
Review
Information
Journal of Developmental Origins of Health and Disease , Volume 7 , Issue 5: Themed Issue: Australia/New Zealand 2015 DOHaD Scientific Meeting: Advances and Updates , October 2016 , pp. 440 - 448
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2016 

A growing body of evidence now links nutrition in early life to an increased risk of disease in adulthood, and the rapid increase in the prevalence of metabolic and allergic disease across the globe. Australia and New Zealand have not been immune to this major health problem.

The risk of developing metabolic and allergic disease is influenced by a range of factors across each individual’s lifespan. Environmental exposures during fetal development and infancy are now considered responsible for a significant part of lifetime disease risk, as they can have long-term effects on both health and disease.

Critical time periods have been identified, both before conception and during fetal and postnatal development, where exposure to environmental factors, including altered nutrition, can cause adaptations to occur in the growing fetus and infant.Reference Jang and Serra 1 , Reference Singhal 2 Although these effects may be adaptive in the short term, they may also be associated with adverse outcomes in childhood and later life, including a greater risk of obesity,Reference Bammann, Peplies and De Henauw 3 type 2 diabetes, heart diseaseReference Roseboom, van der Meulen and Osmond 4 – Reference Eriksson 7 and allergy.Reference Prescott and Saffery 8

Significant contributions to this literature have been made by a number of long-term studies such as the British-based Avon Longitudinal Study of Parents and ChildrenReference Golding 9 , Reference Lawlor, Cooper and Bain 10 and the Dutch-based Generation R Study.Reference Gaillard, Steegers, Franco, Hofman and Jaddoe 11 , Reference Jaddoe, van Dujin and Franco 12

Maternal and paternal nutrition may be important determinants of pregnancy outcomes and the longer term health of the offspring. Furthermore, these effects can be transmitted to subsequent generations, thus perpetuating a cycle of metabolic disorders. Identifying vulnerable periods in fetal and postnatal development provides an important opportunity for parents and healthcare professionals to intervene and optimize future health outcomes.

Nutrition is one of the most easily modifiable environmental factors during early life. It has been shown to influence both fetal and postnatal growth and development,Reference Langley-Evans 13 and the risk of metabolic and allergic disease in childhood and adult life.Reference Bammann, Peplies and De Henauw 3 – Reference Prescott and Saffery 8

This review provides an overview of the importance of early life nutrition, focussing on the situation in Australia and New Zealand.

Impact of maternal and paternal nutrition before conception

It is well accepted that the health of a woman before conception has a significant impact on pregnancy outcomes and thus a lifelong impact on her child’s health. 14 Obesity reduces fertility and affects the health of the human oocyte.Reference Robker 15 Overweight and obesity in women during their reproductive years is of increasing concern. In Australia, over 12 million men and women (~60%) are overweight or obese with that figure having increased by 5% since 1995. Over 30% more people living in outer regional and remote areas are obese than people living in major cities. 16 In New Zealand, there has been an increase in obesity in men from 17% in 1997 to 30% in 2013 and an increase in women from 21 to 32% over the same time period; a further 34% of adults are overweight. There are also marked ethnic disparities with adult obesity rates of 48 and 68% for Maori and Pacific Islanders, respectively. 17

Women who are obese before becoming pregnant are also more likely to develop gestational diabetes (GDM) when pregnant, which in turn increases the risk of diabetes and overweight in the offspring.Reference Torloni, Betrán and Horta 18

Increased paternal body mass index (BMI) has also been linked to impaired embryo and fetal development, as well as reduced pregnancy rates and pregnancy loss.Reference Bakos, Henshaw, Mitchell and Lane 19 – Reference Ramlau-Hansen, Thulstrup and Nohr 22 Conversely, paternal exposure to famine or undernutrition has been associated with a higher BMI in offspring compared with the offspring of fathers who were not exposed to famine.Reference Veenendaal, Painter and de Rooij 23 An animal study involving male rats fed long-term, high-fat diets found that glucose intolerance and impaired insulin secretion developed in their adult female offspring.Reference Ng, Lin and Laybutt 24 These associations between paternal nutrition and health outcomes in the offspring appear to reflect epigenetic changes in the sperm in response to altered nutrition.Reference Lambrot, Xu and Saint-Phar 25

Nutrition during pregnancy

Maternal undernutrition increases metabolic risk in offspring

The Dutch famine provided one of the first insights into the importance of maternal undernutrition and the development of disease in offspring in later life.Reference Roseboom, van der Meulen and Osmond 4 – Reference Painter, de Rooij and Bossuyt 6 , Reference de Rooij, Painter and Roseboom 26 In the Netherlands, there were serious food shortages and a major reduction in daily food intake over a 7-month period during the winter of 1944–1945. Official daily rations for the general adult population fell to between 400 and 800 calories a day. This calorie restriction had a significant impact on the offspring of women who were pregnant at the time, and of note is that the effects differed according to the timing in gestation of the exposure to the famine.

Children born to women exposed to the famine early in the gestation period have been shown to have a significantly greater risk of obesity, heart disease, type 2 diabetes and renal dysfunction 40–50 years later.Reference Roseboom, van der Meulen and Osmond 4 – Reference Painter, de Rooij and Bossuyt 6 , Reference de Rooij, Painter and Roseboom 26 , Reference Ravelli, van der Meulen and Osmond 27 These effects were also transmitted to the second generation.Reference Painter, Osmond and Gluckman 28 This suggests that in the face of energy restriction the fetus becomes conditioned to become highly energy efficient, known as a predictive adaptive response.Reference Bateson, Gluckman and Hanson 29 A child born into a world where food is plentiful, they tend to consume excessive energy because the hunger/satiety set-points have been altered during development, possibly via epigenetic mechanisms.Reference Waterland 30

Maternal obesity, excessive gestational weight gain (GWG), diabetes and stress during pregnancy increase the risk of obesity in the offspring

Several other environmental circumstances have been found to drive obesity in the offspring. These primarily define the ‘set-points’ or sensitivity for obesity and associated risk factors, for example, hunger and satiety, adipose tissue development and metabolism.Reference Gluckman, Lillycrop and Vickers 31 – Reference Heindel and vom Saal 33

Maternal obesity

A 2015 study from Auckland showed that the risk of having an obese mother was double in Maori and Pacific infants compared with New Zealand European infants (OR 2.23 95% CI 1.23–4.04).Reference Howe, Ellison-Loschmann and Pearce 34 Overweight or obese mothers are significantly more likely to have overweight children, with evidence showing that a woman’s BMI at the start of pregnancy is a strong predictor of her offspring’s risk for obesity in adult life.Reference Kim, Sharma and Sappenfield 35 In addition, maternal obesity often precedes GDM.Reference Kim, Sharma and Sappenfield 35 A systematic review found that maternal pre-pregnancy BMI is directly associated with the risk of developing GDM.Reference Torloni, Betrán and Horta 18

Excess GWG

A recently published Australian studyReference Dodd 36 reported that in a cohort of over 2000 women 42% had a GWG above international guidelines, 37 figures similar to previously published smaller studies. In one such study, 38% of Australian women gained more weight during their pregnancy than recommendedReference de Jersey, Nicholson, Callaway and Daniels 38 and in another, 54% of Australian women gained more than recommended (see Table 1).Reference Hure, Collins, Giles, Paul and Smith 39

Recent data from New Zealand are more disturbing still. Over 74% of women in a multicentre study that included Auckland gained more weight during pregnancy than recommended in the international guidelines. Further, 70% of New Zealand woman surveyed were unaware of how much weight gain was appropriate during pregnancy.Reference Fieldwick, Peterson and Stephen 40 Clearly excessive GWG is an important issue to address in Australasia.

The Southampton Women’s Survey found that children born to mothers who gained excessive weight during pregnancy had a greater fat mass at birth and at 6 years than children whose mothers’ GWG was within the recommended range.Reference Crozier, Inskip and Godfrey 41 This study also reported that excessive weight gain in pregnancy was common, and most marked in women who were overweight or obese before becoming pregnant.

The timing of excess weight gain in pregnancy can also affect the health of the offspring. Davenport et al.Reference Davenport, Ruchat and Giroux 42 reported that women following guidelines for healthy living during pregnancy who gained excessive weight during the first half of pregnancy had offspring with a greater heel-crown length, higher birth weight and higher body fat at birth than women who did not gain excessive weight during this time (including those who gained excessive weight during the second half of pregnancy). Excessive weight during the first half of pregnancy was found to be a stronger predictor of excessive body fat in the offspring at birth than total excessive maternal weight gain.Reference Davenport, Ruchat and Giroux 42

Maternal diabetes

Gestational or maternal diabetes mellitus in Australasia is of significant concern. In Australia, analysis of the Midwives Perinatal Data Collection from 2000 to 2009 in over 120,000 indigenous women and nearly 3.5 million non-indigenous women showed a crude prevalence of 5.1 and 4.5%, respectively, a small but highly significant difference (P<0.0001). Moreover, in older (35+ years) indigenous women the crude prevalence of GDM was about 14%.Reference Chamberlain, Banks and Joshy 43 Prevalence rates in New Zealand are also around 5% but appear to have risen from around 3% between 2008 and 2012. 44

Maternal GDM has been shown to result in a number of both short- and long-term complications in offspring,Reference Mitanchez, Yzydorczyk and Siddeek 45 including a greater BMI at 18 years of age.Reference Lawlor, Lichtenstein and Langstrom 46 Recent work by Leng et al.Reference Leng, Li and Zhang 47 examined the association between pre-pregnancy BMI, GWG and anthropometry in the offspring of mothers with GDM. Offspring born to GDM mothers with pre-pregnant overweight or obesity or excessive GWG were associated with increased risks of large for gestational age and macrosomia at birth, and childhood overweight at 1–5 years old, compared with those born to GDM mothers with pre-pregnancy normal weight and adequate GWG.

In addition, animal studies have shown that macrosomic offspring of diabetic mothers exhibit many disorders associated with the metabolic syndrome.Reference Yessoufou and Moutairou 48 , Reference Pereria, Fonseca and Campbell 49

Maternal stress

A study involving Danish army recruits found that those recruits born to mothers bereaved during pregnancy had an overall higher risk of overweight in early adult life than those whose mothers did not. There was also an increased risk of overweight when the mother was bereaved in the 6 months before conception.Reference Hohwü, Li, Olsen, Sørensen and Obel 50

The mechanisms that link maternal obesity, excessive GWG, diabetes and stress during pregnancy to later disease risk in the offspring involve a range of factors. These include epigenetic changes that reset fetal energy metabolism, appetite and adipose tissue development, an abnormal intrauterine environment and poor or restricted placental development.Reference Godfrey, Sheppard and Gluckman 51 , Reference Gardosi 52 These factors, although currently largely associative in nature, may subsequently provide a causal link to the likelihood of developing obesity later in life,Reference Hohwü, Li, Olsen, Sørensen and Obel 50 with the effects of a sedentary lifestyle and modern energy-dense diets exacerbating these effects in affected offspring.

Birth weight is associated with later disease risk

There are clear links between birth weight and subsequent disease risk. While not a causal factor, many studies use birth weight as a proxy measure or clinical marker of the impact of developmental factors on later disease risk. Both low and high birth weights have been associated with an increased risk of childhood and adult obesity, as well as heart disease, stroke and type 2 diabetes later in life.Reference Gluckman, Lillycrop and Vickers 31 , Reference Osmond, Barker and Winter 53 – Reference Osmond, Kajantie and Forsen 57

The United States Nurses’ Health Study involving more than 70,000 women found that in full-term offspring an increased risk of hypertension was associated with low birth weight, whereas an increased risk of obesity was associated with high birth weight.Reference Curhan, Chertow and Willett 58 In birth cohorts from Finland, mortality from stroke and heart disease was greater in people born at a low birth weight.Reference Eriksson, Forsen and Tuomilehto 56 , Reference Osmond, Kajantie and Forsen 57 A British study involving more than 15,000 people found that death rates from heart disease fell with increasing birth weight.Reference Osmond, Barker and Winter 53 , Reference Barker, Osmond, Winter, Margetts and Simmonds 59

Although overweight and obesity, excessive GWG and GDM are all associated with large for gestational age infants,Reference Kim, Sharma and Sappenfield 35 maternal obesity can also lead to low birth weight infants. A New Zealand retrospective analysis of more than 26,000 pregnancies found that maternal obesity was an independent risk factor for small-for-gestational age infants.Reference Anderson, Sadler and Stewart 60 Several mechanisms may account for these counter intuitive findings, including a reduced likelihood that intrauterine growth restriction is detected and acted upon in obese mothers.Reference Gardosi 52 Further, animal studies suggest that a maternal high-fat diet may lead to fetal growth restriction due to placental insufficiency and reduced nutrient transport.Reference Mark, Sisala and Connor 61

Influence of maternal macronutrient intake on appetite and food preferences in the offspring

Programming of appetite and food preferences may occur during fetal development. A study comparing maternal nutrient intake of protein, fat and carbohydrate during pregnancy with the maternal, paternal and child dietary intake of the same nutrients following birth found that the maternal diet during pregnancy was most strongly associated with later childhood intake (assessed at 10 years of age) of the same nutrients, particularly protein and fat. This association was greater than those observed for postnatal paternal and maternal intake, suggesting that some programming of appetite in the offspring may occur during fetal development.Reference Brion, Ness and Rogers 62

Maternal carbohydrate intake has also been associated with alterations in epigenetic markers at birth and later childhood.Reference Godfrey, Sheppard and Gluckman 51

A study involving the Dutch famine cohort found that the offspring of mothers exposed to famine in early gestation were twice as likely to consume a high-fat diet in later life.Reference Lussana, Painter and Ocke 63 Experimental models have also shown that alterations in the maternal nutritional environment can programme altered appetite and food preferences in offspring.Reference Gugusheff, Ong and Muhlhauser 64 For example, a reduction in maternal protein intake can result in a preference for high-fat foods in offspringReference Langley-Evans, Bellinger and McMullen 65 and maternal undernutrition can lead to persistent hyperphagia in offspring in later life.Reference Vickers, Breier, Cutfield, Hoffman and Gluckman 66

Early life nutrition affects the developing immune system and risk of allergic disease

Early life nutrition has a substantial impact on the developing immune system, which is highly sensitive to environmental changes. Although many immune system disorders are inherited, genetic factors alone cannot explain the dramatic rise in many immune diseases in recent years. For example, Australia has one of the highest rates of food allergy in the worldReference Prescott and Allen 67 and there have been reports that there has been a 10-fold increase in specialist referrals for food allergy and a five-fold increase hospitalization for food-related anaphylaxis in recent years.Reference Mullins 68

Surprisingly, there are few if any good data on the prevalence of food allergy in New Zealand. It has been suggested, however, that based on the similar rates of asthma in New Zealand, Australia, the United Kingdom and the United States that the prevalence of food allergy might also be similar to that in Australia. 69 These changes, particularly the rise in food allergy, highlight the vulnerability of the developing immune system to early environmental exposure.Reference Jaddoe, van Dujin and Franco 12 , Reference Langley-Evans 13

Allergic disease may be manifest very early in life, often in the first few months after birth. There are demonstrated differences in the immune function of newborns that develop allergic disease compared with those who do not, suggesting that alterations in immune system function begin during fetal development.Reference Prescott and Saffery 8 , Reference Prescott 70 , Reference Prescott and Clifton 71 A range of environmental cues have been shown to influence immune development and function, including maternal nutrition, microbial burden and pollutants such as cigarette smoke.

In addition, the rising rates of maternal allergy – itself a risk factor for the development of allergic disease in the offspring – may further amplify the effects of environmental exposures on the developing immune system.Reference Prescott and Saffery 8 Women with a history of allergy appear to have altered immune interactions with their fetus, so that the fetal immune response to environmental cues may be modified.Reference Prescott and Saffery 8 In addition, maternal allergy is a stronger predictor of allergic risk in offspring than paternal allergy.Reference Prescott and Saffery 8

Some maternal nutritional changes have been associated with altered immune programming. These include a reduced intake of omega 3 polyunsaturated fatty acids, folate and zinc.Reference Langley-Evans 13 The recently released Australian Bureau of Statistics/Food Standards Australia New Zealand Australian Health Survey: Usual Nutrient Intakes, 2011–12, 72 reveals that about 10% of women aged 19–50 years have an inadequate intake of folate and between 10 and 15% of women in the same age range have an inadequate intake of zinc.

The LISA PLUS study, a prospective study involving more than 3000 infants, found that a high maternal intake of margarine, vegetable oils and some fruits and vegetables (celery, citrus fruit, sweet peppers) during pregnancy may be associated with an increased risk of allergies, especially eczema.Reference Sausenthaler, Heinrish and Koletzko 73

Gut colonization and microbial diversity in the offspring differs between vaginal and caesarean delivery,Reference Azad, Konya and Maughan 74 which may have an impact on the later development of allergic disease;Reference Kolokotroni, Middleton and Gavatha 75 breastfeeding also influences the establishment of the gut microbiota. Low gut microbial diversity and disturbances in gut colonization patterns during infancy and childhood have been associated with later onset of allergic disease.Reference Abrahamsson, Jakobsson and Andersson 76 , Reference Ismail, Oppedisano and Joseph 77

The rate of fetal growth may affect allergy risk. In the UK Southampton birth cohort, rapid fetal abdominal growth between 11 and 19 weeks’ gestation followed by slowing of abdominal growth was associated with later atopy.Reference Pike, Crozier and Lucas 78

Other key maternal nutritional factors that alter the risk of allergic disease and obesity in the offspring

Several other key nutrients, including antioxidants (selenium, zinc, vitamins A, C, D and E), long-chain polyunsaturated fatty acids (LCPUFA) and pre- and probiotics have been linked to multiple health outcomes, including asthma and allergic disease and obesity. The recent Australia New Zealand Australian Health Survey: Usual Nutrient Intakes, 2011–12 72 shows that vitamin A deficiency is around 26% in 14–18-year-old women but falls to around 15–20% in women aged 19–50 years. The number of women with an inadequate intake of vitamin C and selenium is low, being around 5%. Data for vitamin D and vitamin E were not reported.

Antioxidants

In vitro studies in human macrophages have shown that antioxidants can favourably improve immune function.Reference Utsugi, Dobashi and Ishizuka 79 Observational studies suggest that higher dietary intakes of antioxidant-rich foods, such as fresh fruit and vegetables, or higher antioxidant levels measured in pregnancy may reduce the risk of wheezing, asthma and/or eczema in the offspring,Reference Devereux, Turner and Craig 80 although there is inconsistency in the evidence.Reference Martindale, McNeill and Devereux 81

LCPUFA

Dietary omega 3 LCPUFA have been shown to have multisystem anti-inflammatory benefits in terms of immune and metabolic outcomes. Several randomized control trials of maternal fish oil supplementation during pregnancy have found beneficial immunomodulatory effects in terms of reduced allergen sensitization and allergic disease outcomes in the offspring.Reference Dunstan, Mori and Barden 82 – Reference Prescott, Barden, Mori and Dunstan 84 Other studies have shown beneficial effects on metabolic programming and cardiovascular risk with higher dietary intakes of omega 3 LCPUFA in early life.Reference Innis 85 – Reference Skilton, Ayer and Harmer 87

Vitamin D

There is consistent geographical variation in the prevalence of vitamin D status, which has been associated with the incidence of allergic disease. Specifically, a low prevalence of allergic disease is seen in equatorial regions (where vitamin D levels are generally higher), and a higher prevalence of allergic disease with increasing distance from the equator (where vitamin D levels are typically lower).Reference Kimlin 88 This association is reported for food allergy, eczema and asthma.Reference Camargo, Clark and Kaplan 89 – Reference Krstic 91 A systematic review and meta-analysisReference Aghajafari, Nagulesapillai and Ronksley 92 concluded that vitamin D insufficiency during pregnancy is associated with an increased risk of GDM, pre-eclampsia and small-for-gestational age infants. A recent Australian cohort study of infants with a parental history of allergic disease found that lower cord blood vitamin D concentrations were significantly associated with eczema at 1 year of age.Reference Jones, Palmer, Zhang and Prescott 93 Vitamin D deficiency in pregnancy had been called a potential ‘threat’ to the child, an indication of the perceived importance of vitamin D status during this time.Reference Savendahl 94 Moreover, a 2014 publication from South Australia revealed that an inadequate vitamin D status (<50 nmol/l) was present in about 21% of women aged 24–34 years and in about 27% of women aged 35–44 years.Reference Gill, Hill and Shanahan 95

Prebiotics and probiotics

Modern diets typically contain more processed, low-fibre foods and less fruit, vegetables, unprocessed grains, nuts and seeds.Reference Cordain, Eaton and Sebastian 96 , Reference Kuhnlein and Receveur 97 This dietary pattern is associated with changes in gut microbial biodiversity, another common risk factor now strongly linked with both allergy and obesity.Reference Renz, Brandtzaeg and Hornef 98 The maternal gut microbial environment is also emerging as a potential risk/protective factor for allergy in the offspring, with maternal microbial transfer to the fetus likely to begin during pregnancy. This early exposure may help to prepare the fetus for extensive microbial exposure during vaginal delivery and after birth.Reference Rautava, Luoto and Salminen 99 A healthy balance of specific microorganisms in the gut is essential for healthy immune system development; infants who develop allergic disease have an altered balance of gut microorganisms in early life.Reference Nauta, Ben Amor and Knol 100 , Reference Nylund, Satokari and Nikkila 101 Animal models have shown that gut microbiota modulate immune programming and can reduce the risk of allergic disease as well as the risk of obesity, cardiovascular disease and other metabolic disease.Reference Renz 102 – Reference Turnbaugh, Ley and Mahowald 104 Similarly, the use of soluble ‘prebiotic’ fibre (oligosaccharides) has been shown to have beneficial effects on both immune status and metabolic homoeostasis.Reference van Hoffen, Ruiter and Faber 105 , Reference Cani, Possemiers and Van de Wiele 106

Nutrition during the first years of the life

It is not just health and nutrition during pre-conception and pregnancy that can impact on later disease risk. Exposures during infancy and as toddlers can also affect the risks of developing allergic and metabolic disease in later life.

During the early months after birth, nutrition is provided in the form of milk – either human milk via breastfeeding or formula milk via bottle feeding when breastfeeding is not possible. There are long-term health benefits in infants who are breastfed for any length of time, including protection against some immune-mediated disorders,Reference Dogaru, Nyffenegger and Pescatore 107 a reduced risk of obesityReference Arenz, Ruckerl and Koletzko 108 as well as positive effects on cognitive function.Reference Kramer, Aboud and Mironova 109 Breastfed babies may also gain weight at a slower rate than formula-fed babies, which has implications for the subsequent reduced risk of overweight and obesity.

Although infant-feeding guidelines have typically recommended exclusive breastfeeding until around 6 months of age, 110 there is emerging evidence that introducing solids after 17 weeks (~4 months) and before 6 months of age (while continuing breastfeeding) has potential benefits in terms of reducing the risk of some food allergies.Reference Du Toit, Katz and Sasieni 111 – Reference Koplin, Osborne and Wake 113 There may be a time window for the child to develop appropriate immunological gut tolerance beginning at around 4 months of age.Reference Prescott, Smith and Tang 112 In line with these findings, the Australasian Society of Clinical Immunology and Allergy 114 has advised relaxing recommendations to avoid certain food groups and allow the introduction of solid foods after 17 weeks, while continuing breastfeeding. The ideal time to introduce solids is a topic of significant debate, and it may be too soon to draw definite conclusions, although most recommendations state that it is important that the introduction of solids does not occur before 17 weeks of age, before which the infant may not be developmentally ready to be able to consume solids. Moreover, two recent reviews found that introducing solid foods any earlier may increase the risk of childhood overweight or obesity, although the evidence is not strong.Reference Pearce, Taylor and Langley-Evans 115 , Reference Daniels, Mallan, Fildes and Wilson 116 A recent contemporary Australian study based in Queensland reported that in a group of first-time mothers, 21% had given their infant non-milk foods before 17 weeks of age.Reference Newby and Davies 117

The composition and quality of milk and early solid foods may also influence changes in BMI and lead to obesity.Reference Weber, Grote and Closa-Monasterolo 118 For example, a high intake of protein during infancy has been linked to obesity in childhood. The Childhood Obesity Project compared lower protein and higher protein content formula (both levels within recommended ranges) during the first year of life.Reference Weber, Grote and Closa-Monasterolo 118 The study found that infants fed the higher protein content formula had a significantly higher BMI at 6 years of age and a greater risk of obesity. Although the optimal upper limit of dietary protein intake has not been firmly established, a systematic review found that a higher protein intake (i.e. comprising 15–20% of energy intake) in infancy and early childhood was associated with increased growth and an increased risk of being overweight in later childhood.Reference Hörnell, Lagström, Lande and Thorsdottir 119

The rate of growth during infancy influences metabolic risk in later life

Weight gain during the first year of life, often in the form of rapid ‘catch-up’ growth, is a strong predictor of later obesity risk.Reference Baird, Fisher and Lucas 120 , Reference Monteiro and Victora 121 Moreover, in premature infants at least, the rate of early growth in infancy has been related to long-term cardiovascular health.Reference Singal, Cole, Fewtrell, Deanfield and Lucas 122

This, however, has to be considered in the light of evidence that rapid growth and ‘aggressive’ nutrition in such infants is associated with improved cognitive function in childhood.Reference Ziegler, Thureen and Carlson 123

Importance of early eating patterns and behaviours

The first 2–3 years after birth are critical times for programming of long-term energy regulation, especially establishing patterns of healthy nutrition and physical activity.124 It is also a key time during which a child’s taste patterns and food preferences are set. Importantly, children’s eating and lifestyle behaviours are heavily influenced by parenting practices. Young children may be at greater risk of becoming overweight or obese due to parental modelling of behaviours that predispose children to weight gain.124

Conclusion

Nutrition and lifestyle factors throughout pre-conception, pregnancy, infancy and early childhood have a profound influence on a child’s development and long-term health.

The evidence contained in this publication is designed to assist healthcare professionals in their efforts to maximize this critical window of opportunity when the foundations of future health are created.

As the findings of further research become available, recommendations for optimizing early life nutrition should be formulated and made widely available as part of the preventative health policy agenda in both Australia and New Zealand.

Table 1

Recommended weight gain during pregnancy 37

Acknowledgements

The authors acknowledge the assistance from Sue Markham, Medical and Science writer at Superscript Medical Writing who collated the authors input and drafted an initial report for critical review and revision by the authors, as well as the assistance of John Morton from Ethical Strategies who played a coordination, facilitation and administration role for the initial meeting of the authors and also kept a version control of the document.

Financial Support

The authors also acknowledge that the initial meeting of the authors was organized by Nutricia/Danone Australia/New Zealand. Nutricia/Danone funded accommodation, flights, where required, and an honorarium to each member of the ANZ Early Life Nutrition Working Party for their attendance at the meeting, but had no input into the original document, the current manuscript or the recommendations therein. The production of this manuscript was supported via a donation to the Children’s Nutrition Research Centre, University of Queensland from Nutricia/Danone.

Conflicts of Interest

None.

References

1. Jang, H, Serra, C. Nutrition, epigenetics and diseases. Clin Nutr Res. 2014; 3, 1–8.Google Scholar
2. Singhal, A. The global epidemic of noncommunicable disease: the role of early-life factors. Nestle Nutr Inst Workshop Ser. 2014; 78, 123–132.Google Scholar
3. Bammann, K, Peplies, J, De Henauw, S, et al. Early life course risk factors for childhood obesity: the IDEFICS case-control study. PLoS One. 2014; 9, 1–7.Google Scholar
4. Roseboom, T, van der Meulen, JHP, Osmond, C, et al. Coronary heart disease after prenatal exposure to the Dutch famine, 1944–45. Heart. 2000; 84, 595–598.CrossRefGoogle Scholar
5. Roseboom, T, de Rooij, S, Painter, R. The Dutch famine and its long-term consequences for adult health. Early Hum Dev. 2006; 82, 485–491.Google Scholar
6. Painter, RC, de Rooij, SR, Bossuyt, PM, et al. Early onset of coronary artery disease after prenatal exposure to the Dutch famine. Am J Clin Nutr. 2006; 84, 322–327.Google Scholar
7. Eriksson, JG. Epidemiology, genes and the environment: lessons learned from the Helsinki Birth Cohort Study. J Intern Med. 2007; 261, 418–425.Google Scholar
8. Prescott, S, Saffery, R. The role of epigenetic dysregulation in the epidemic of allergic disease. Clin Epigenetics. 2011; 2, 223–232.Google Scholar
9. Golding, J. The Avon Longitudinal Study of Parents and Children (ALSPAC) – study design and collaborative opportunities. Eur J Endocrinol. 2004; 151, U119–U123.Google Scholar
10. Lawlor, DA, Cooper, AR, Bain, C, et al. Associations of birth size and duration of breast feeding with cardiovascular fitness in childhood: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC). Eur J Epidemiol. 2008; 23, 411–422.Google Scholar
11. Gaillard, R, Steegers, EAP, Franco, OH, Hofman, A, Jaddoe, VWV. Maternal weights gain in different periods of pregnancy and childhood cardio-metabolic outcomes. The Generation R Study. Int J Obes. 2015; 39, 677–685.Google Scholar
12. Jaddoe, VWV, van Dujin, CM, Franco, OH, et al. The Generation R Study. Design and cohort update 2012. Eur J Epidemiol. 2012; 27, 739–756.Google Scholar
13. Langley-Evans, SC. Nutrition in early life and the programming of adult disease: a review. J Hum Nutr Diet. 2015; 28(Suppl. 1), 1–14.Google Scholar
14. Royal Australian and New Zealand College of Obstetricians and Gynaecologists. Pre-pregnancy Counselling. College Statement C-Obs 3 (a). Current: November 2012.Google Scholar
15. Robker, RL. Evidence that obesity alters the quality of oocytes and embryos. Pathophysiology. 2008; 15, 115–121.Google Scholar
16. Australian Institute of Health and Welfare. Obesity, 2014. Retrieved December 2014 from http://www.aihw.gov.au/overweight-and-obesity/ Google Scholar
17. Ministry of Health New Zealand Survey. Obesity key facts and statistics, 2012/2013. Retrieved December 2014 from http://www.health.govt.nz/our-work/diseases-and-conditions/obesity/obesity-key-facts-and-statistics Google Scholar
18. Torloni, AP., Betrán, BL, Horta, MU, et al. Prepregnancy BMI and the risk of gestational diabetes: a systematic review of the literature with meta-analysis. Obes Rev. 2009; 10, 194–203.CrossRefGoogle ScholarPubMed
19. Bakos, HW, Henshaw, RC, Mitchell, M, Lane, M. Paternal body mass index is associated with decreased blastocyst development and reduced live birth rates following assisted reproductive technology. Fertil Steril. 2011; 95, 1700–1704.Google Scholar
20. Keltz, J, Zapantis, A, Jindal, SK, et al. Overweight men: clinical pregnancy after ART is decreased in IVF but not in ICSI cycles. J Assist Reprod Genet. 2010; 27, 539–544.Google Scholar
21. Nguyen, RH, Wilcox, AJ, Skjaerven, R, Baird, DD. Men’s body mass index and infertility. Hum Reprod. 2007; 22, 2488–2493.Google Scholar
22. Ramlau-Hansen, CH, Thulstrup, AM, Nohr, EA, et al. Subfecundity in overweight and obese couples. Hum Reprod. 2007; 22, 1634–1637.Google Scholar
23. Veenendaal, MVE, Painter, RC, de Rooij, SR, et al. Transgenerational effects of prenatal exposure to the 1944–45 Dutch famine. BJOG. 2013; 120, 548–554.Google Scholar
24. Ng, SF, Lin, RC, Laybutt, DR, et al. Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring. Nature. 2010; 467, 963–966.Google Scholar
25. Lambrot, RI, Xu, C, Saint-Phar, S, et al. Low paternal dietary folate alters the mouse sperm epigenome and is associated with negative pregnancy outcomes. Nat Commun. 2013; 4, 2889.Google Scholar
26. de Rooij, SR, Painter, RC, Roseboom, TJ, et al. Glucose tolerance at age 58 and the decline of glucose tolerance in comparison with age 50 in people prenatally exposed to the Dutch famine. Diabetologia. 2006; 49, 637–643.Google Scholar
27. Ravelli, ACJ, van der Meulen, JHP, Osmond, C, et al. Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr. 1999; 70, 811–816.Google Scholar
28. Painter, RC, Osmond, C, Gluckman, P, et al. Transgenerational effects of prenatal exposure to the Dutch famine on neonatal adiposity and health in later life. BJOG. 2008; 115, 1243–1249.Google Scholar
29. Bateson, P, Gluckman, PD, Hanson, M. The biology of developmental plasticity and the redictive adaptive response. J Physiol. 2014; 592(11), 2357–2368.Google Scholar
30. Waterland, RA. Epigenetic mechanisms affecting regulation of energy balance: many questions, few answers. Annu Rev Nutr. 2014; 34, 337–355.Google Scholar
31. Gluckman, PD, Lillycrop, KA, Vickers, MH, et al. Metabolic plasticity during mammalian development is directionally dependent on early nutritional status. Proc Natl Acad Sci USA. 2007; 104, 12796–12800.Google Scholar
32. Gluckman, PD, Hanson, MA, Cooper, C, Thornburg, KL. Effect of in utero and early-life conditions on adult health and disease. N Engl J Med. 2008; 359, 61–73.Google Scholar
33. Heindel, JJ, vom Saal, FS. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Mol Cell Endocrinol. 2009; 304, 90–96.Google Scholar
34. Howe, LD, Ellison-Loschmann, L, Pearce, N, et al. Ethnic differences in risk factors for obesity in New Zealand infants. J Epidemiol Community Health. 2015; 69, 516–522.Google Scholar
35. Kim, SY, Sharma, AJ, Sappenfield, W, et al. Association of maternal body mass index, excessive weight gain, and gestational diabetes mellitus with large-for-gestational-age births. Obstet Gynecol. 2014; 123, 737–744.Google Scholar
36. Dodd, JM. Dietary and lifestyle advice for pregnant woman who are overweight or obese: the LIMIT randomised trial. Ann Nutr Metab. 2014; 64, 197–202.Google Scholar
37. Institute of Medicine. Weight gain during pregnancy: re examining the guidelines. 2009. National Academies Press: Washington, DC.Google Scholar
38. de Jersey, SJ, Nicholson, JM, Callaway, LK, Daniels, LA. A prospective study of pregnancy weight gain in Australian women. Aust N Z J Obstet Gynaecol. 2012; 52, 545–551.Google Scholar
39. Hure, AJ, Collins, CE, Giles, WB, Paul, JW, Smith, R. Greater maternal weight gain during pregnancy predicts a large but lean fetal phenotype: a prospective study. Matern Child Health J. 2012; 16, 1374–1384.Google Scholar
40. Fieldwick, D, Peterson, H, Stephen, M, et al. Management of excess weight in pregnancy in Otago, New Zealand: a qualitative study with lead maternity cares. N Z Med J. 2014; 127(1392), 27–37.Google Scholar
41. Crozier, SR, Inskip, HM, Godfrey, KM, et al. Weight gain in pregnancy and childhood body composition: findings from the Southampton Women’s Survey. Am J Clin Nutr. 2010; 91, 1745–1751.Google Scholar
42. Davenport, MH, Ruchat, S-M, Giroux, I, et al. Timing of excessive pregnancy-related weight gain and offspring adiposity at birth. Obstet Gynecol. 2013; 122, 255–261.Google Scholar
43. Chamberlain, C, Banks, E, Joshy, G, et al. Prevalence of gestational diabetes mellitus among Indigenous women and comparison with non Indigenous Australian women: 1990-2009. Aust N Z J Obstet Gynaecol. 2014; 54, 433–440.Google Scholar
44. Ministry of Health New Zealand. Diabetes, 2013. Retrieved December 2014 from https://www.health.govt.nz/your-health/conditions-and-treatments/diseases-and-illnesses/diabetes.Google Scholar
45. Mitanchez, D, Yzydorczyk, C, Siddeek, B, et al. The offspring of the diabetic mother – short and long term implications. Best Pract Res Clin Obstet Gynaecol. 2015; 29, 256–269.Google Scholar
46. Lawlor, DA, Lichtenstein, P, Langstrom, N. Association of maternal diabetes mellitus in pregnancy with offspring adiposity into early adulthood: sibling study in a prospective cohort of 280 866 men from 248 293 families. Circulation. 2011; 123, 258–265.Google Scholar
47. Leng, J, Li, W, Zhang, S, et al. GDM womens pre-pregnancy overweight/obesity and gestational weight gain on offspring overweight status. PLoS One. 2015; 10, 1–15.Google Scholar
48. Yessoufou, A, Moutairou, K. Maternal diabetes in pregnancy: early and long-term outcomes on the offspring and the concept of ‘metabolic memory’. Exp Diabetes Res. 2011; 1–12.Google Scholar
49. Pereria, TJ, Fonseca, MA, Campbell, KE, et al. Maternal obesity characterized by gestational diabetes increases the susceptibility of rat offspring to hepatic steatosis via a disrupted liver metabolome. J Physiol. 2015; 14, 3181–3197.Google Scholar
50. Hohwü, L, Li, J, Olsen, J, Sørensen, TI, Obel, C. Severe maternal stress exposure due to bereavement before, during and after pregnancy and risk of overweight and obesity in young adult men: a Danish national cohort study. PLoS One. 2014; 9, e97490.Google Scholar
51. Godfrey, KM, Sheppard, A, Gluckman, PD, et al. Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes. 2011; 60, 1528–1534.Google Scholar
52. Gardosi, J. Intrauterine growth restriction: new standards for assessing adverse outcome. Best Pract Res Clin Obstet Gynaecol. 2009; 23, 741–749.Google Scholar
53. Osmond, C, Barker, DJ, Winter, PD, et al. Early growth and death from cardiovascular disease in women. BMJ. 1993; 307, 1519–1524.Google Scholar
54. Gluckman, PD, Hanson, MA. Living with the past: evolution, development, and patterns of disease. Science. 2004; 305, 1733–1736.Google Scholar
55. Gluckman, PD, Hanson, MA, Low, FM. The role of developmental plasticity and epigenetics in human health. Birth Defects Res C Embryo Today. 2011; 93, 12–18.Google Scholar
56. Eriksson, JG, Forsen, T, Tuomilehto, J, et al. Early growth, adult income, and risk of stroke. Stroke. 2000; 31, 869–874.Google Scholar
57. Osmond, C, Kajantie, E, Forsen, TJ, et al. Infant growth and stroke in adult life. The Helsinki birth cohort study. Stroke. 2007; 38, 264–270.CrossRefGoogle ScholarPubMed
58. Curhan, GC, Chertow, GM, Willett, WC, et al. Birth weight and adult hypertension and obesity in women. Circulation. 1996; 94, 1310–1315.Google Scholar
59. Barker, DJP, Osmond, C, Winter, PD, Margetts, B, Simmonds, SJ. Weight in infancy and death from ischaemic heart disease. Lancet. 1989; 2, 577–580.Google Scholar
60. Anderson, NH, Sadler, LC, Stewart, AW, et al. Independent risk factors for infants who are small for gestational age by customised birthweight centiles in a multi-ethnic New Zealand population. Aust N Z J Obstet Gynaecol. 2013; 53, 136–142.Google Scholar
61. Mark, PJ, Sisala, C, Connor, K, et al. A maternal high fat diet in rat pregnancy reduces growth of the fetus and the placental junctional zone, but not placental labyrinth zone growth. J Dev Orig Health Dis. 2011; 2(1), 63–70.Google Scholar
62. Brion, M-J, Ness, AR, Rogers, I, et al. Maternal macronutrient and energy intakes in pregnancy and offspring intake at 10 y: exploring parental comparisons and prenatal effects. Am J Clin Nutr. 2010; 91, 748–756.Google Scholar
63. Lussana, F, Painter, RC, Ocke, MC, et al. Prenatal exposure to the Dutch famine is associated with a preference for fatty foods and a more atherogenic lipid profile. Am J Clin Nutr. 2008; 88(6), 1648–1652.CrossRefGoogle Scholar
64. Gugusheff, JR, Ong, ZY, Muhlhauser, BS. The early origins of food preferences: targeting the critical windows of development. FASEB. 2015; 29, 365–373.Google Scholar
65. Langley-Evans, SC, Bellinger, L, McMullen, S. Animal models of programming: early life influences on appetite and feeding behaviour. Matern Child Nutr. 2005; 1, 142–148.Google Scholar
66. Vickers, MH, Breier, BH, Cutfield, WS, Hoffman, PC, Gluckman, PD. Fetal origins of hyperphagia, obesity and hypertension and postnatal amplification of hypercaloric nutrition. Am J Physiol. 2000; 279(1), E83–E87.Google Scholar
67. Prescott, S, Allen, KJ. Food allergy: riding the second wave of the allergy epidemic. Pediatr Allergy Immunol. 2011; 22, 155–160.Google Scholar
68 Mullins, RJ. Paediatric food allergy trends in a community based specialist allergy practice. Med J Aus. 2007; 186, 618–621.CrossRefGoogle Scholar
69. Allergy New Zealand. Food allergy, 2015. Retrieved December 2014 from http://www.allergy.org.nz/site/allergynz/What%20is%20the%20prevalence%20of%20food%20allergy%20in%20New%20Zealand.pdf Google Scholar
70. Prescott, SL. Early origins of allergic disease: a review of processes and influences during early immune development. Curr Opin Allergy Clin Immunol. 2003; 3, 125–132.Google Scholar
71. Prescott, SL, Clifton, VL. Asthma and pregnancy: emerging evidence of epigenetic interactions in utero. Curr Opin Allergy Clin Immunol. 2009; 9, 417–426.Google Scholar
72. Australian Bureau of Statistics/Food Standards Australia New Zealand. Australian Health Survey: usual nutrient intakes, Commonwealth of Australia, 2011-12 4364.0.55.008. 2015.Google Scholar
73. Sausenthaler, S, Heinrish, J, Koletzko, S, for the GINIplus and LISDA plus study groups. Early diet and the risk of allergy: what can we learn from the prospective birth cohort studies GINIplus and LISAplus? Am J Clin Nutr. 2011; 94, 212S–217S.Google Scholar
74. Azad, MB, Konya, T, Maughan, H, et al. Gut microbiota of healthy Canadian & infants: profiles by mode of delivery and infant diet at 4 months. CMAJ. 2013; 185, 385–394.Google Scholar
75. Kolokotroni, O, Middleton, N, Gavatha, M, et al. Asthma and atopy in children born by caesarean section: effect modification by family history of allergies: a population based cross-sectional study. BMC Pediatr. 2012; 12, 179.Google Scholar
76. Abrahamsson, TR, Jakobsson, HE, Andersson, AF, et al. Low diversity of the gut microbiota in infants with atopic eczema. J Allergy Clin Immunol. 2012; 129, 434–440.Google Scholar
77. Ismail, IH, Oppedisano, F, Joseph, SJ, et al. Reduced gut microbial diversity in early life is associated with later development of eczema but not atopy in high-risk infants. Pediatr Allergy Immunol. 2012; 23, 674–681.Google Scholar
78. Pike, KC, Crozier, SR, Lucas, JSA, et al. Patterns of fetal and infant growth are related to atopy and wheezing disorders at age 3 years. Thorax. 2010; 65, 1099–1106.CrossRefGoogle ScholarPubMed
79. Utsugi, M, Dobashi, K, Ishizuka, T, et al. c-Jun N-terminal kinase negatively regulates lipopolysaccharide-induced IL-12 production in human macrophages: role of mitogen-activated protein kinase in glutathione redox regulation of IL-12 production. J Immunol. 2003; 171, 628–635.Google Scholar
80. Devereux, G, Turner, SW, Craig, LC, et al. Low maternal vitamin E intake during pregnancy is associated with asthma in 5-year-old children. Am J Respir Crit Care Med. 2006; 174, 499–507.Google Scholar
81. Martindale, S, McNeill, G, Devereux, G, et al. Antioxidant intake in pregnancy in relation to wheeze and eczema in the first two years of life. Am J Respir Crit Care Med. 2005; 171, 121–128.Google Scholar
82. Dunstan, JA, Mori, TA, Barden, A, et al. Fish oil supplementation in pregnancy modifies neonatal allergen-specific immune responses and clinical outcomes in infants at high risk of atopy: a randomized, controlled trial. J Allergy Clin Immunol. 2003; 112, 1178–1184.Google Scholar
83. Palmer, DJ, Sullivan, T, Gold, MS, et al. Effect of n-3 long chain polyunsaturated fatty acids (LCPUFA) supplementation in pregnancy on infant allergies in the first year of life: a randomised controlled trial. BMJ. 2012; 344, e184.Google Scholar
84. Prescott, SL, Barden, AE, Mori, TA, Dunstan, JA. Maternal fish oil supplementation in pregnancy modifies neonatal leukotriene production by cord-blood-derived neutrophils. Clin Sci. 2007; 113, 409–416.Google Scholar
85. Innis, SM. Metabolic programming of long-term outcomes due to fatty acid nutrition in early life. Matern Child Nutr. 2011; 7(Suppl. 2), 112–123.Google Scholar
86. Forsyth, JS, Willatts, P, Agostoni, C, et al. Long chain polyunsaturated fatty acid supplementation in infant formula and blood pressure in later childhood: follow up of a randomised controlled trial. BMJ. 2003; 326, 953.Google Scholar
87. Skilton, MR, Ayer, JG, Harmer, JA, et al. Impaired fetal growth and arterial wall thickening: a randomized trial of omega-3 supplementation. Pediatrics. 2012; 29, e698–e703.Google Scholar
88. Kimlin, M. Geographic location and vitamin D synthesis. Mol Aspects Med. 2008; 29, 453–461.Google Scholar
89. Camargo, CAJ, Clark, S, Kaplan, MS, et al. Regional differences in EpiPen prescriptions in the United States: the potential role of vitamin D. J Allergy Clin Immunol. 2007; 120, 131–136.Google Scholar
90. Weiland, SK, Husing, A, Strachan, DP, et al. Climate and the prevalence of symptoms of asthma and atopic eczema in children.. Occup Environ Med. 2004; 61, 609–615.Google Scholar
91. Krstic, G. Asthma prevalence associated with geographical latitude and regional insolation in the United States of America and Australia. PLoS One. 2011; 6, e18492.Google Scholar
92. Aghajafari, F, Nagulesapillai, T, Ronksley, PE, et al. Association between maternal serum 25-hydroxyvitamin D level and pregnany and neonatal outcomes: systematic review and meta analysis of observational studies. BMJ. 2013; 346, f1169.Google Scholar
93. Jones, AP, Palmer, D, Zhang, G, Prescott, SL. Cord blood 25-hydroxyvitamin D3 and allergic disease during infancy. Pediatrics. 2012; 130, e1128–e1135.Google Scholar
94. Savendahl, L. Vitamin D deficiency during pregnancy-potential threat to the child. Acta Paediatr. 2011; 100, 484–485.Google Scholar
95. Gill, TK, Hill, CL, Shanahan, EM, et al. Vitamin D levels in an Australian population. BMC Public Health. 2014; 14, 1001.CrossRefGoogle Scholar
96. Cordain, L, Eaton, SB, Sebastian, A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005; 81, 341–354.Google Scholar
97. Kuhnlein, HV, Receveur, O. Dietary change and traditional food systems of indigenous peoples. Annu Rev Nutr. 1996; 16, 417–442.Google Scholar
98. Renz, H, Brandtzaeg, P, Hornef, M. The impact of perinatal immune development on mucosal homeostasis and chronic inflammation. Nat Rev Immunol. 2012; 12, 9–23.Google Scholar
99. Rautava, S, Luoto, R, Salminen, S, et al. Microbial contact during pregnancy, intestinal colonization and human disease. Nat Rev Gastroenterol Hepatol. 2012; 9, 565–576.Google Scholar
100. Nauta, AJ, Ben Amor, K, Knol, J, et al. Relevance of pre- and postnatal nutrition to development and interplay between the microbiota and metabolic and immune systems. Am J Clin Nutr. 2013; 98, 586S–593S.Google Scholar
101. Nylund, L, Satokari, R, Nikkila, J, et al. Microarray analysis reveals marked intestinal microbiota aberrancy in infants having eczema compared to healthy children in at-risk for atopic disease. BMC Microbiol. 2013; 13, 12.Google Scholar
102. Renz, H. Development and regulation of immune responses in pre- and postnatal life. Clin Biochem. 2011; 44, 495.Google Scholar
103. Sudo, N, Sawamura, S, Tanaka, K, et al. The requirement of intestinal bacterial flora for the development of an IgE production system fully susceptible to oral tolerance induction. J Immunol. 1997; 159, 1739–1745.Google Scholar
104. Turnbaugh, PJ, Ley, RE, Mahowald, MA, et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006; 444, 1027–1031.Google Scholar
105. van Hoffen, E, Ruiter, B, Faber, J, et al. A specific mixture of short-chain galacto-oligosaccharides and long-chain fructo-oligosaccharides induces a beneficial immunoglobulin profile in infants at high risk for allergy. Allergy. 2009; 64, 484–487.Google Scholar
106. Cani, PD, Possemiers, S, Van de Wiele, T, et al. Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut. 2009; 58, 1091–1103.Google Scholar
107. Dogaru, CM, Nyffenegger, D, Pescatore, AM, et al. Breastfeeding and Childhood Asthma: Systematic Review and Meta-Analysis. Am J Epidemiol. 2014; 179, 1153–1169.Google Scholar
108. Arenz, S, Ruckerl, R, Koletzko, B, et al. Breast-feeding and childhood obesity – a systematic review. Int J Obes. 2004; 28, 1247–1256.Google Scholar
109. Kramer, MS, Aboud, F, Mironova, E, et al. Breastfeeding and child cognitive development: new evidence from a large randomized trial. Arch Gen Psychiatry. 2008; 65, 578–584.Google Scholar
110. National Health and Medical Research Council. Infant Feeding Guidelines. 2012. National Health and Medical Research Council: Canberra.Google Scholar
111. Du Toit, G, Katz, Y, Sasieni, P, et al. Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy. J Allergy Clin Immunol. 2008; 122, 984–991.Google Scholar
112. Prescott, SL, Smith, P, Tang, M, et al. The importance of early complementary feeding in the development of oral tolerance: concerns and controversies. Pediatr Allergy Immunol. 2008; 19, 375–380.Google Scholar
113. Koplin, JJ, Osborne, NJ, Wake, M, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol. 2010; 126, 807–813.Google Scholar
114. Australasian Society of Clinical Immunology and Allergy. Infant feeding advice, 2010. Retrieved December 2014 from www.allergy.org.au/content/view/350/287.Google Scholar
115. Pearce, J, Taylor, MA, Langley-Evans, SC. Timing of the introduction of complementary feeding and risk of childhood obesity: a systematic review. Int J Obes. 2013; 37, 1295–1306.Google Scholar
116. Daniels, L, Mallan, KM, Fildes, A, Wilson, J. The timing of solid introduction in an obesogenic environment: a narrative review of the evidence and methodological issues. Aust N Z J Public Health 2015; 39, 366–373.Google Scholar
117. Newby, R, Davies, PSW. Introduction of complementary foods in contemporary Australian infants: what, when and why. J Paediatr Child Health. 2015; 51(2), 186–191.Google Scholar
118. Weber, M, Grote, V, Closa-Monasterolo, R, et al. Lower protein content in infant formula reduces BMI and obesity risk at school age: follow-up of a randomized trial. Am J Clin Nutr. 2014; 99, 1041–1051.Google Scholar
119. Hörnell, A, Lagström, H, Lande, B, Thorsdottir, I. Protein intake from 0 to 18 years of age and its relation to health: a systematic literature review for the 5th Nordic Nutrition Recommendations. Food Nutr Res. 2013; 57, 1–42.Google Scholar
120. Baird, J, Fisher, D, Lucas, P, et al. Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ. 2005; 331, 929.Google Scholar
121. Monteiro, PO, Victora, CG. Rapid growth in infancy and childhood and obesity in later life – a systematic review. Obes Rev. 2005; 6, 143–154.Google Scholar
122. Singal, A, Cole, TC, Fewtrell, M, Deanfield, J., Lucas, A. Is slower early growth beneficial for long term cardiovascular health? Circulation. 2004; 109, 1108–1113.Google Scholar
123. Ziegler, EE, Thureen, PJ, Carlson, SJ. Aggressive nutrition of the very low birthweight infant. Clin Perinatol. 2002; 29, 225–244.Google Scholar
124. National Health and Medical Research Council. Clinical Practice Guidelines for the Management of Overweight and Obesity in Adults, Adolescents and Children in Australia. 2013. National Health and Medical Research Council: Melbourne.Google Scholar
Figure 0

Table 1 Recommended weight gain during pregnancy37