IJE Advance Access originally published online on July 15, 2006
International Journal of Epidemiology 2006 35(5):1196-1210; doi:10.1093/ije/dyl130
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Article |
Are infant size and growth related to burden of disease in adulthood? A systematic review of literature
1 MRC Epidemiology Resource Centre, University of Southampton, Southampton General Hospital, Southampton, UK
2 Freelance information specialist
3 School for Policy Studies, University of Bristol, Bristol, UK
4 Child Health Research and Policy Unit, Institute of Health Sciences, City University, London, UK
5 Centre for Reviews and Dissemination, University of York, York, UK
6 Centre for Policy Research, Centre for Paediatric Epidemiology and Biostatistics, Institute of Child Health, University College London, London, UK
7 Present address: Kleijnen Systematic Reviews Ltd, York, UK
* Corresponding author. Catherine Law, Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK. E-mail: C.Law{at}ich.ucl.ac.uk
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Abstract |
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Background Slower rates of infant growth are associated with increased rates of death from ischaemic heart disease (IHD) in later life. We carried out a systematic review to assess the association between infant size or growth and leading causes of adult burden of disease to contribute to the debate on the potential of the promotion of infant growth to prevent ischaemic heart disease.
Methods We searched Medline, Embase, CINAHL, PsycINFO, and bibliographies of included studies. First authors of included studies and other experts were contacted to locate unpublished analyses. Outcome measures for the review were leading causes of adult burden of disease selected from the Global Burden of Disease study. We included studies that assessed the relationship between infant size or growth during the first 2 years and the leading causes of adult burden of disease.
Results Nineteen studies relating to 10 causes of burden of disease met inclusion criteria. Most studies reported data on infant size. Larger size in infancy was associated with increased risk of insulin-dependent diabetes. Larger infant size was associated with reduced rates of IHD in men but not in women. There were considerable gaps in the evidence and many conditions that account for a high burden of disease, such as cancer, mental illness, stroke, chronic obstructive pulmonary disease, and non-insulin-dependent diabetes, had few or no studies associating them with infant size or growth.
Conclusions Our findings suggest that there is no single optimal pattern of infant growth that is associated with beneficial adult health outcomes. There is insufficient evidence to recommend prevention of adult disease through strategies to alter infant growth.
Keywords Infant, growth, adult, chronic disease
Accepted 25 May 2006
Observational evidence links slower rates of infant growth and smaller infant size to increased rates of death from ischaemic heart disease (IHD) in later life.1,2 This suggests a role for interventions to promote infant size or growth in the prevention of IHD. As IHD is one of the leading causes of burden of disease in developed countries,3 such interventions might have a large impact on public health.4 However, the potential effect of changes in infant growth on other leading causes of burden of disease, such as stroke, depression, and cancer, has not been assessed.
Collation of evidence is a pre-requisite to developing an intervention or policy. If alteration of infant growth is proposed as a strategy for preventing adult disease, this collation needs to consider the likely balance of benefits and harms associated with such an intervention,5 a matter of importance to both parents and policy makers. There is already some evidence suggesting that infant growth may be linked to adverse outcomes: more rapid growth in infancy is linked to higher rates of obesity6 and obesity is a risk factor for a number of important causes of burden of disease, including diabetes and cancer.
To contribute to the debate on the potential of the promotion of infant growth to prevent IHD, we have carried out a systematic review to assess the relationship between infant growth and leading causes of adult burden of disease. Previous systematic reviews in this field have tended to assess the relationship of an early life exposure with a single disease or risk factor in later life.7,8 We have considered a range of outcomes that reflect the total burden of adult disease.
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Methods |
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The systematic review described in this paper was part of a wider review of scientific evidence on infant growth and health and well-being across the life course, which was carried out alongside a review of lay perspectives on infant growth supplemented by individual and focus group interviews.
We sought studies relating measures of individuals' infant size or growth to at least one of a range of adult outcomes. Studies of infant size were eligible for inclusion if they reported at least one measurement of infant size between 3 months and 2 years of age. Studies of infant growth needed to report at least 2 measurements of size up to 2 years of age, of which at least one was between 3 months and 2 years. We did not impose any limits in relation to study timing, setting, or language. We excluded ecological studies and non-human studies, but did not impose any other limits on study design.
Outcomes were chosen on the basis of their contribution to burden of disease. Our source of outcomes was the Global Burden of Disease Study (GBDS), which ranked leading causes of death and disability in 1990 and reported projections for the year 2020, summarized using disability adjusted life years (DALYs).3 We used the 2020 projections as these are more relevant to today's infants who would be the target population of an intervention to alter early growth. We selected the 10 outcomes accounting for the greatest number of DALYs in developed countries for men or women, giving 12 outcomes in total (Table 1).
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We searched Medline and Embase from their start dates to June 2005 for all outcomes and also CINAHL and PsycINFO for studies concerning mental illness outcomes. Separate search strategies were used for each outcome. We used many search terms for both the exposure, infant size or growth, and the outcomes in order to maximize the sensitivity of our searches.9 The bibliographies of all included studies were hand-searched. We contacted first authors of all included studies and other experts in the field to identify further published or unpublished analyses.
We followed the methods recommended by the Centre for Reviews and Dissemination (CRD)10 Two reviewers independently assessed each title and abstract for potential relevance to the review. Potentially relevant papers were obtained and assessed in detail against review inclusion criteria. Disagreements over inclusion were resolved through consensus and, where necessary, through discussion with a third member of the review team. Study quality was assessed independently by two reviewers using a checklist of questions. The questions used, while based on CRD guidelines, were developed in an iterative process of extensive piloting and through consultation with the review expert advisory group. Two separate checklists were devised, one for studies using a case–control design and one for other studies (mostly cohort studies). A number of aspects of quality (11 for cohort and 12 for case–control designs) were assessed according to whether they posed a low, medium, or high risk of bias for study results.9 Aspects of quality assessed included appropriateness of study design, ascertainment of exposure and outcome, consideration of the effects of important confounding factors, rates of attrition, and approach to statistical analysis. Overall judgement on study quality, as summarized in Tables 2
–7, was based on the combination of performance in the checklist and consensus between the two independent reviewers. Our approach to synthesis was mainly narrative but we explored the potential for meta-analysis according to standard procedures.10
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Results |
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TopAbstractMethodsResultsDiscussionStrengths and weaknessesComparison with other researchImplications for policy and...References |
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Overall
We identified 73 314 abstracts. Screening of abstracts and reference lists identified 49 potentially relevant studies. Detailed assessment of these 49 papers revealed that 19 studies, relating to 10 outcomes, met inclusion criteria. The most common reason for exclusion was that measurements of size or growth did not fall within the 3 month to 2 year time period specified in the inclusion criteria.9 Most of the included studies reported data on infant size. Only four studies presented growth data. The evidence for 7 of the 10 outcomes where we identified studies related mainly to mortality. Two studies were set in a developing country (India), with the remainder set in developed countries (UK, Northern Europe, or USA). All studies were observational, including 12 cohort studies. The results of most studies were assessed as having medium risk of bias in relation to the review question. Only two studies were judged to have low risk of bias and three had high risk of bias. The most frequent sources of bias were high attrition rates, inadequate consideration of confounding, and lack of information on the original source population and those lost to follow-up.
Table 1 shows the number of results reported for each direction of association of increased size with a particular outcome found in the 17 studies of infant size. The outcomes are ordered according to their relative contribution to burden of disease as reported in the GBDS.3 A statement of statistical significance, for example a confidence interval or P-value, was required for study findings to be categorized as ‘inverse’, ‘positive’, or ‘none’. If this was not given, or if results were inconsistent, then the findings were categorized as ‘inconclusive’. It was not possible to carry out meta-analysis for any outcome because of the small numbers of studies for individual outcomes and because the definitions of both the exposures (infant size and growth) and outcomes varied between studies.
Results are presented within sections for each outcome. Each section gives a brief description of the studies, the definitions used for each outcome and for infant size or growth, aspects of quality, and their results. Where studies adjusted for important confounding factors, this is noted in the size of effect column.
Insulin-dependent diabetes
The GBDS reports diabetes mellitus as a single disease.3 As the aetiology of non-insulin-dependent diabetes (NIDDM) may differ from that of insulin-dependent diabetes (IDDM), we have considered their relationship with infant growth and size separately.
Seven studies of infant size or growth and IDDM were identified (Table 2). Six were based in developed countries and one in India. Since IDDM is chronic, we included studies of IDDM at any age. Five studies used a case–control design and were based on childhood and adolescent cases (<15 years). Two were cross-sectional, measuring size at the time of diagnosis (in infancy). All the studies included male and female subjects in roughly equal proportions.
Six studies reported data on infant size. Four were case–control and two were cross-sectional studies. Two case–control studies set in Finland obtained infant weight measurements at ages between 3 months and 2 years. Neither study was considered to have a high risk of bias and both reported positive associations between weight during the first 2 years of life and risk of later IDDM in both sexes.11,12 The other two case–control studies were considered to have a high risk of bias. Of these, one set in the UK reported a significant positive association between infant weight and later IDDM among males (but not females) at 6 months and among females (but not males) at 12 months,13 while the other, set in Holland, suggested that IDDM cases had higher body mass index (BMI) at 1 year than a healthy comparison group but the controls did not (no data were presented and so only the infant growth findings for this study are displayed in Table 2).14
The two cross-sectional studies only included very early-onset cases by design.15,16 Both reported data on infant height. The Wisconsin study, which had medium risk of bias, suggested that at 1 year, infant height was lower for cases than controls particularly males.15 The other cross-sectional study, set in India and judged to have a high risk of bias, suggested that cases were taller than controls at both 1 and 2 years, with the difference being greater among females, but no statistical analysis was reported.16
Two case–control studies reported findings relating to infant growth.14,17 In one study, based in Sweden, which had medium risk of bias, cases had significantly increased infant growth compared with controls over nearly all time periods measured.17 The other study, based in Holland and with high risk of bias, suggested that BMI of cases increased more quickly than that of controls during the first year, but that growth in height was similar in cases and controls.14
Taking into account the relative sample sizes and risks of bias posed by the studies, infant size and growth appear to be positively associated with risk of IDDM.
Non-insulin-dependent diabetes
Of three cohort studies of infant size and NIDDM (Table 3), one was based on males from Hertfordshire, UK,18 and another was based on men and women born in Helsinki, Finland, during 1934–44.19 The third study was based on subjects born 1969–72 in a region of India.20 The Hertfordshire study measured weight at 1 year, while the other two studies calculated z-scores throughout childhood for subjects with NIDDM. All three studies examined prevalence of NIDDM. All had large sample sizes and were considered to have medium or low risk of bias.
The Hertfordshire study presented prevalence of newly diagnosed NIDDM between 59 and 70 years of age within categories of infant weight and suggested that the risk of NIDDM reduced with increasing weight, although no statistical analysis was reported.18 The Finland study suggested that cases of later NIDDM were slightly smaller in infancy than the cohort as a whole, as measured by weight, height or BMI, but these differences were not significant.19 The Indian study reported no significant associations between size (height, weight, and BMI) at 2 years and NIDDM.20
In summary, there is some suggestion that adults with NIDDM were of smaller size in infancy than comparison groups, since all the studies reported results in the same direction. However, none was statistically significant.
Ischaemic heart disease
Four cohort studies (described in five publications) related infant size or growth to IHD (Table 4). Subjects were aged between 53 and 80 years of age at the time of follow-up. One study based in Hertfordshire, UK, considered mortality from IHD21; two based in Finland (one of males and one of females) used hazard ratios for mortality or morbidity2,22; and the fourth study (restricted to males), which was also based on the Hertfordshire cohort, examined IHD morbidity using a Rose angina questionnaire and ECG findings.23 The three mortality studies were large scale2,21,22 but the morbidity study was smaller.23 All studies were assessed as medium risk of bias.
The Hertfordshire mortality study reported hazard ratios for mortality from IHD according to infant size (weight at 1 year) and growth up to 1 year,21 while the morbidity study reported percentage prevalence for IHD across subgroups categorized according to weight at 1 year.23 The Finland studies reported hazard ratios for mortality or morbidity from IHD by weight, height, and BMI at 1 year.2,22 Findings were consistent across studies: men who were smaller (in terms of weight, but also height and BMI where these were reported) in infancy experienced significantly greater mortality and morbidity from IHD as adults, while no such association was found in women. The Hertfordshire mortality study found that increased growth from birth to 1 year was associated with increased risk of IHD in men but not women.21 A combined analysis of the men and women in the two Finland studies2,22 suggested that increased growth in BMI up to 2 years of age was associated with reduced levels of adult IHD.24
Cancer
Two cohort studies of cancer were identified (Table 5). One was based on deaths from lung cancer among the same Hertfordshire population reviewed previously.21 The other examined breast cancer morbidity in women aged 36–54 years who were participants in the UK's Medical Research Council National Survey of Health and Development (NSHD).25
The Hertfordshire study did not show an association between weight at 1 year or growth from birth to 1 year and risk of mortality from lung cancer in either males or females.21 The study of breast cancer did not show an association between size at 2 years and breast cancer prevalence, though this might be partly attributed to the lack of cases of breast cancer in a relatively young cohort of women.25 Both studies had medium risk of bias.
Mental illness
Two cohort studies were identified that related infant size to mental illness in adulthood, based on the same Hertfordshire cohort as the IHD studies (Table 6). One study reported a significant inverse association between infant size and adult mortality from suicide in males and females combined. However, when the sexes were considered separately, the association was only significant in males. There was also a significant increased risk of suicide associated with poorer infant growth among men but this was not significant in women.26 The other study of mental illness reported no significant association between infant size and morbidity from adult depression after adjustment for socioeconomic status, birthweight, and presence of IHD.27 Both studies had medium risk of bias.
Other outcomes
A single study was identified for each of osteoarthritis, cerebrovascular disease, chronic obstructive pulmonary disease (COPD), dementia, and Alzheimer's disease. All studies were cohort studies set in the UK and all had medium risk of bias.
One study of osteoarthritis was identified, based on men and women who were part of the NHSD birth cohort (Table 7). Weight at 2 years of age was not related to prevalence of osteoarthritis of the hand at 53 years.28
The single study of cerebrovascular disease (Table 7) explored the relationship between weight at 1 year and risk of mortality from stroke in Hertfordshire men.29 Infant size was inversely associated with risk of death from stroke in males.
A single publication on the Hertfordshire cohort reported data on mortality from COPD, dementia, and Alzheimer's disease (Table 7).21 Hazard ratios for mortality for a 1 SD increase in weight at 1 year and growth in weight from birth to 1 year were given. Increases in both infant size and growth were associated with a decreased rate of mortality from COPD in males, but there was no significant association for females. Associations with dementia were inconclusive—a positive association was found between infant size and death from dementia among males, but the association with growth was non-significant and there were no associations among females. No significant associations were found with mortality from Alzheimer's disease in either sex.21
No studies were found that included relevant data for road traffic accidents or alcohol use.
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Discussion |
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TopAbstractMethodsResultsDiscussionStrengths and weaknessesComparison with other researchImplications for policy and...References |
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We found evidence that larger infant size is associated with reduced rates of IHD in adult men: those who were of smaller size in infancy experienced greater mortality and morbidity from IHD as adults. No association was demonstrated in women, but there was evidence from a single study that greater gain in BMI in the first 2 years is associated with reduced rates of IHD in both men and women. There were also single studies suggesting that larger size in infancy is associated with lower rates of stroke and COPD. However, the studies reporting beneficial effects of larger infant size were largely based on two cohorts of adults (Hertfordshire and Finland) born 60 or more years ago and were published by a single research group. Our findings also suggest that larger size in infancy is associated with increased risk of IDDM. The association between infant size and IDDM was demonstrated consistently in studies from a range of settings and researchers. For 7 of the 10 outcomes where studies were identified, the evidence related mainly to disease mortality rather than morbidity. In general, whether studies considered mortality or morbidity was dependent on the outcomes being considered and the study design. So, for example, most studies of IHD were mortality studies based on retrospective cohorts. Conversely, most studies of IDDM were case–control studies of morbidity.
We found considerable gaps in the evidence. Conditions such as cancer, mental illness, stroke, dementia, road traffic accidents, and NIDDM, which account for a high burden of disease and disability, had few or no studies associating them with infant size or growth. Much debate has focused on whether it is attained size or the pattern of growth that is associated with later disease.30 However, most of the studies we reviewed considered infant size, particularly weight, and very few considered the relationship between infant growth and adult disease.
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Strengths and weaknesses |
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TopAbstractMethodsResultsDiscussionStrengths and weaknessesComparison with other researchImplications for policy and...References |
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Our review used rigorous and standard methods10 and was supported by an expert advisory group. The outcomes we considered were based on the GBDS, which attempts to quantify the burden of different diseases in a common unit of DALYs.3 This enabled us to select outcomes that were the leading causes of DALYs. In addition to the GBDS outcomes, we considered including risk factors for these outcomes, such as blood pressure or respiratory function. However, the risk factors for certain diseases (such as cardiovascular disease) are better characterized than others (such as cancer), and therefore including risk factors in our review might have over emphasized the evidence on cardiovascular disease.
There were a number of challenges in interpreting the evidence in this review. Most studies had at least a medium risk of bias in relation to the review question. Rates of attrition and consideration of confounding, were the two aspects of quality where studies were most often considered to have high risk of bias. This may be due to the observational nature of the studies we were considering, particularly since many were historical cohort studies that considered mortality and are likely to have had little information about confounding factors. These findings concur with those of recent research, which suggested that many published epidemiological studies do not deal adequately with confounding.31 Our systematic searches encompassed a wide range of sources. Despite this extensive search for studies, the literature was dominated by three cohort studies for most of the outcomes we considered: the British NSHD, the Hertfordshire (UK), and the Helsinki (Finland) cohorts. Therefore, the outcomes studied may reflect the research interests of the groups working on these cohorts and the findings may partly reflect specific features of the cohort members or settings. Cohort studies of adult outcomes are necessarily conducted on people whose infancy occurred decades ago. Their generalizability to infants growing up now may be limited. They are likely to have had different experiences of infancy, for example with respect to breastfeeding and burden of infection. We did not assume causality in the relationships that we examined, recognizing that infant growth is one of a number of inter-related factors that may be associated with later health and disease, including infant feeding and socioeconomic status. Infant growth may be an indicator of other factors rather than causing observed associations.
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Comparison with other research |
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As far as we are aware, no previous review has considered the relationship of any early outcome (including infant size and growth) with adult burden of disease. Previous reviews have focused on birthweight or childhood growth and have tended to consider outcomes as single disease groups or risk factors, such as cancers, obesity, and blood pressure, rather than considering a range of outcomes.7,32,33 For example, a review of breast cancer and childhood growth found evidence of a positive association between height in childhood and adolescence and prevalence of or mortality from breast cancer later in life, although, as with our review, important confounding factors were often unaccounted for.33
Debate has also focused on the size of effect of associations between early life factors and later outcomes.7 The high number of outcomes considered in the wider review of infant growth and health across the life course meant that it was not feasible to obtain data from study authors to carry out secondary analyses as has been done in previous systematic reviews of early life exposures and single outcomes. Although quantification of the relationship of an early life exposure and a single outcome is valuable, it may be insufficient to inform policy development, which, arguably, needs to consider all dimensions of people's lives across the whole of the life course.
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Implications for policy and practice |
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TopAbstractMethodsResultsDiscussionStrengths and weaknessesComparison with other researchImplications for policy and...References |
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Our findings suggest that there is no single optimal pattern of infant growth that is associated with beneficial adult health outcomes. While there is some evidence to suggest that increasing infant size might have benefits in reducing rates of IHD, the evidence also suggests potential for harm given that larger infant size is associated with increased rates of IDDM. Our review has also exposed many gaps in the evidence base. Little is known about the relationship of infant size or growth with many outcomes that are responsible for substantial burden of disease in adulthood such as depression and cancer. This is a cause for concern for some outcomes where an association with infant growth is biologically plausible. For example, breast cancer and NIDDM have been linked to other early life exposures such as birthweight. Most of the evidence we reviewed related to infant size rather than infant growth, limiting our ability to assess whether it is rate of infant growth or actual size that is associated with risk of disease.
These gaps are important. Policy makers and clinicians will be reluctant to advise on patterns of infant growth when there is uncertainty about risk of harm, and interventions to alter infant growth are unlikely to be acceptable to parents or professionals without stronger evidence to support their development and introduction. Future research should focus on addressing the gaps identified by this review.
KEY MESSAGES
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Acknowledgments |
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We would like to thank our advisory group for their input to the project and, especially, Paul Dieppe for chairing it. We would also like to thank colleagues at Medical Research Council Epidemiology Resource Centre, University of Southampton, Institute of Child Health, University College London, and the Centre for Reviews and Dissemination, University of York for their assistance and support. We are grateful to the unknown reviewers of our original proposal and final report to the Department of Health for their helpful comments. We thank the experts and first authors of papers who we contacted for their assistance. This project was funded by the Department of Health. The views expressed in this report are those of the authors and not necessarily those of the Department of Health. J.B. is an MRC Special Training Fellow in Health Services and Health of the Public Research. The sponsor of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication. C.L., J.B., H.R., and J.K. obtained funding. All authors were responsible for the concept and design of the study. J.B., D.F., P.L., and L.P. carried out the review work with assistance from C.L., H.R., and J.K. All authors were responsible for the interpretation of findings. D.F., J.B., and C.L. produced the first draft of this paper and all authors were responsible for critical revision of the manuscript. C.L. is guarantor.
Conflict of interest statement
We declare that we have no conflict of interest.
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References |
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1 Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet 1989;2:577–80.[Web of Science][Medline]
2 Eriksson JG, Forsen T, Tuomilehto J, Osmond C, Barker DJ. Early growth and coronary heart disease in later life: longitudinal study. BMJ 2001;322:949–53.
3 Murray CJL, Lopez AD. Regional patterns of disability-free life expectancy and disability-adjusted life expectancy: Global Burden of Disease Study. Lancet 1997;349:1347–52.[CrossRef][Web of Science][Medline]
4 Barker DJP, Eriksson JG, Forsen T, Osmond C. Fetal origins of adult disease: strength of effects and biological basis. Int J Epidemiol 2002;31:1235–39.
5 Campbell M, Fitzpatrick R, Haines A et al. Framework for design and evaluation of complex interventions to improve health. BMJ 2000;321:413–19.
6 Baird J, Fisher D, Lucas P, Kleijnen J, Roberts H, Law CM. Being big or growing fast: a systematic review of size and growth in infancy and later obesity. BMJ 2005; doi:10.1136/bmj.38586.411273.E0 (published 14 October 2005).
7 Huxley RR, Neil A, Collins R. Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure? Lancet 2002;360:659–65.[CrossRef][Web of Science][Medline]
8 Owen CG, Martin RM, Whincup PH, Davey Smith G, Gillman MW, Cook DG. The effect of breastfeeding on mean body mass index throughout life: a quantitative review of published and unpublished observational evidence. Am J Clin Nutr 2005;82:1298–307.
9 Baird J, Lucas P, Fisher D, Kleijnen J, Roberts H, Law CM. Defining optimal infant growth for lifetime health: a systematic review of lay and scientific literature. Available at: http://www.mrc.soton.ac.uk/index.asp?page=176.
10 NHS Centre for Reviews and Dissemination. Undertaking systematic reviews of research on effectiveness: CRD's guidance for those carrying out or commissioning reviews. CRD Report No. 4 (2nd Edition). York: Centre for Reviews and Dissemination, 2001.
11 Hypponen E, Kenward MG, Virtanen SM et al. Infant feeding, early weight gain, and risk of type I diabetes. Diabetes Care 1999;22:1961–65.
12 Hypponen E, Virtanen SM, Kenward MG, Knip M, Akerblom HK. Childhood Diabetes in Finland Study Group. Obesity, increased linear growth, and risk of type 1 diabetes in children. Diabetes Care 2000;23:1755–60.
13 Baum JD, Ounsted M, Smith MA. Letter: weight gain in infancy and subsequent development of diabetes mellitus in childhood. Lancet 1975;2:866.[Web of Science][Medline]
14 Bruining GJ. Association between infant growth before onset of juvenile type-1 diabetes and autoantibodies to IA-2. Netherlands Kolibrie study group of childhood diabetes.[see comment]. Lancet 2000;356:655–56.[CrossRef][Web of Science][Medline]
15 DiLiberti JH, Carver K, Parton E, Totka J, Mick G, McCormick K. Stature at time of diagnosis of type 1 diabetes mellitus. Pediatrics 2002;109:479–83.
16 Ramachandran A, Snehalatha C, Joseph TA, Vijay V, Viswanathan M. Height at onset of insulin-dependent diabetes in children in southern India. Diabetes Res Clin Pract 1994;23:55–57.[CrossRef][Web of Science][Medline]
17 Johansson C, Samuelsson U, Ludvigsson J. A high weight gain early in life is associated with an increased risk of type 1 (insulin-dependent) diabetes mellitus. Diabetologia 1994;37:91–94.[Web of Science][Medline]
18 Hales CN, Barker DJP, Clark PMS et al. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ 1991;303:1019–22.
19 Eriksson JG, Forsen T, Tuomilehto J, Osmond C, Barker DJ. Early adiposity rebound in childhood and risk of Type 2 diabetes in adult life. Diabetologia 2003;46:190–94.[Web of Science][Medline]
20 Bhargava SK, Sachdev HS, Fall CH et al. Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. New Engl J Med 2004;350:865–75.
21 Syddall HE, Sayer AA, Simmonds SJ et al. Birth weight, infant weight gain and cause-specific mortality: The Hertfordshire cohort study. Am J Epidemiol 2005;161:1074–80.
22 Forsen T, Osmond C, Eriksson JG, Barker DJ. Growth of girls who later develop coronary heart disease. Heart 2004;90:20–24.
23 Fall CH, Vijayakumar M, Barker DJ, Osmond C, Duggleby S. Weight in infancy and prevalence of coronary heart disease in adult life. BMJ 1995;310:17–19.
24 Barker DJP, Osmond C, Forsen T, Kajantie E, Eriksson JG. Trajectories of growth among children who later develop coronary heart disease or its risk factors. New Engl J Med 2005;353:1802–09.
25 De Stavola BL, dos Santos Silva I, McCormack V, Hardy RJ, Kuh DJ, Wadsworth ME. Childhood growth and breast cancer. Am J Epidemiol 2004;159:671–82.
26 Barker DJ, Osmond C, Rodin I, Fall CH, Winter PD. Low weight gain in infancy and suicide in adult life. BMJ 1995;311:1203.
27 Thompson C, Syddall H, Rodin I, Osmond C, Barker DJ. Birth weight and the risk of depressive disorder in late life. Br J Psychiatry 2001;179:450–55.
28 Sayer AA, Poole J, Cox V et al. Weight from birth to 53 years: a longitudinal study of the influence on clinical hand osteoarthritis. Arthritis Rheum 2003;48:1030–33.[CrossRef][Web of Science][Medline]
29 Martyn CN, Barker DJ, Osmond C. Mothers' pelvic size, fetal growth, and death from stroke and coronary heart disease in men in the UK. Lancet 1996;348:1264–68.[CrossRef][Web of Science][Medline]
30 Lucas A, Fewtrell MS, Cole TJ. Fetal origins of adult disease—the hypothesis revisited. BMJ 1999;319:245–49.
31 Pocock SJ, Collier TJ, Dandreo KJ et al. Issues in the reporting of epidemiological studies: a survey of recent practice. BMJ 2004; doi:10.1136/bmj.38250.571088.55 (published 6 October 2004).
32 Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a systematic review. Int J Obes Relat Metab Disord 1999;23:S1–107.
33 Okasha M, McCarron P, Gunnell D, Davey Smith G. Exposures in childhood, adolescence and early adulthood and breast cancer risk: a systematic review of literature. Breast Cancer Res Treat 2003;78:223–76.[CrossRef][Web of Science][Medline]
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S. EBRAHIM Entelechy, citation indexes, and the association of ideas Int. J. Epidemiol., October 1, 2006; 35(5): 1117 - 1118. [Full Text] [PDF]
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