IJE Advance Access originally published online on April 27, 2007
International Journal of Epidemiology 2007 36(4):907-915; doi:10.1093/ije/dym067
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Cardiovascular risk factors at age 30 following pre-term birth
1Clinical Trials Research Unit, The University of Auckland, Auckland, New Zealand.
2Liggins Institute, The University of Auckland, Auckland, New Zealand.
*Corresponding author. Liggins Institute, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail: harding{at}auckland.ac.nz
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Abstract |
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Background Recent epidemiological evidence has shown increased rates of cardiovascular mortality and associated risk factors in those born small. However, scarce information exists concerning cardiovascular risk factors in adulthood following pre-term birth, or distinguishing the relative contributions of length of gestation and fetal growth to small size at birth.
Methods Prospective follow-up of 458 30-year-olds whose mothers took part in a randomized controlled trial of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome (147 born at term, 311 born pre-term). Follow-up assessments included anthropometry, blood pressure, blood lipids, early morning cortisol levels and 75 g oral glucose tolerance test.
Results Gestational age at birth, pre-term birth, and birth weight z-score were not associated with serum cholesterol, triglyceride or cortisol at age 30 (P > 0.1 for all). However, pre-term birth was associated with increased systolic blood pressure (3.5 mmHg, 95% CI 0.9–6.1 mmHg, P = 0.009) and insulin resistance at age 30 [Log (Insulin area under the curve) = 0.17, 95% CI 0.05–0.28, P = 0.006]. Low gestational age at birth was also associated with these outcomes, whereas birth weight, adjusted for gestational age, was not.
Conclusions Adults who were born moderately pre-term have increased blood pressure and insulin resistance at 30 years of age. Pre-term birth rather than poor fetal growth is the major determinant of this association. As both the incidence of pre-term birth and survival amongst those born pre-term are increasing, this group may contribute an increasing proportion to overall cardiovascular disease burden.
Keywords Pre-term birth, birth weight, developmental origins of adult disease, cardiovascular risk, long-term follow-up
Accepted 13 March 2007
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Introduction |
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Cardiovascular disease and its key determinants of high blood pressure, cholesterol, body mass and type 2 diabetes, are major contributors to global disease burden.1 Over the past two decades, a large amount of epidemiological evidence has shown increased rates of cardiovascular mortality and associated risk factors in those born small,2 although there is uncertainty about the size of these associations.3,4 Specifically, low birth weight has been associated with later increased blood pressure, increased plasma cholesterol and cortisol levels and impaired glucose and insulin metabolism.3–6 However, the studies reporting these findings have failed to adequately distinguish between the contributions of length of gestation and fetal growth to size at birth. This is mainly due to the use of historical retrospective cohorts that lack prospective information on length of gestation and/or cohorts comprised mainly of individuals born at term that include very few pre-term individuals. Yet pre-term birth remains the major determinant of low birth weight.7
There have been few reports of blood pressure, plasma lipids, hypothalamic-pituitary-adrenal (HPA) axis function and insulin/glucose axis function in adulthood following pre-term birth. This is partly because survival rates after pre-term birth were very low before the 1970s, so that most large well-defined cohorts of pre-term survivors have not yet reached adulthood. Furthermore, the cohorts of pre-term survivors that have developed since the 1970s have generally focused attention on neurodevelopmental sequelae and been restricted to those of very low birth weight, despite the fact that the majority of pre-term survivors are born at gestations of >32 weeks and birth weights of >1500 g.7
Currently, up to 12% of all live births occur before 37 completed weeks gestation, with those born at <32 weeks or <1500 g only accounting for 2.0% and 1.5%, respectively.8 The majority of pre-term babies now survive, so that ex-pre-term survivors are rapidly becoming a substantial proportion of the adult population, particularly in developed countries. If this group has increased susceptibility to cardiovascular risk in adulthood, as suggested from the relationships between low birth weight and later increased cardiovascular risk in the historical and term cohorts, then determining the relative contributions of length of gestation and fetal growth to such risk may help inform both public health and obstetric policy.
Administration of antenatal glucocorticoids was one of the first treatments shown to substantially reduce mortality and morbidity in infants born pre-term.9 The survivors of the first randomized controlled trial of this treatment (the Auckland Steroid Trial)10,11 are now in their thirties. All women enrolled into the original trial were considered to be at risk of pre-term delivery. However, approximately one-third delivered at term, and most of the remainder delivered at what would now be considered only moderately pre-term gestations. Their surviving offspring therefore comprise a unique cohort whose perinatal history, including birth weight and gestational age, was recorded prospectively, and who have now survived into adulthood.
We have previously reported that exposure to antenatal betamethasone resulted in signs of insulin resistance but had no effect on body size, fasting lipids, blood pressure, plasma cortisol, prevalence of diabetes or history of cardiovascular disease in this cohort.12 The aim of this current study was to determine the independent contributions of gestational length and fetal growth, explored as birth weight standard deviation (z) scores (i.e. birth weight independent of gestational age), on cardiovascular risk factors at age 30.
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Methods |
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Auckland steroid trial
The Auckland steroid trial and follow-up have been described previously.10–13 Briefly, between December 1969 and February 1974, all women expected to deliver between 24 and 36 weeks at National Women's Hospital, Auckland, New Zealand, were eligible for enrolment unless immediate delivery was indicated. Women were randomized to an intramuscular injection of 6 mg short-acting betamethasone phosphate and 6 mg long-acting betamethasone acetate or an identical-appearing placebo of 6 mg cortisone acetate with one-seventieth of the glucocorticoid potency (trial 1). The allocated treatment was repeated once 24 h later if delivery had not occurred. If possible, labour was arrested with tocolytics for 48 h. After the first 717 women had enrolled, the dose of betamethasone was doubled (trial 2). A total of 1142 women were enrolled, and delivered 1218 babies. Of the 988 neonatal survivors at 28 days of age, 349 (35%) had been born at term. The incidence of term delivery seen is similar to current practice.9
Thirty-year follow-up
Between February 2002 and December 2003, attempts were made to trace those ‘babies’, now adults, who survived the neonatal period. Those located were invited to enter a follow-up study of adult cardiovascular risk factors.12 Participants completed a questionnaire recording occupation, education, income, physical activity, alcohol and tobacco consumption, past medical history and parental medical history. Participants who resided in New Zealand, or were returning to New Zealand within the study timeframe, attended a clinic, or were seen in their own home, for further investigations. A study nurse blinded to participants, perinatal characteristics and antenatal betamethasone exposure, recorded anthropometric measures using standardized techniques.14 Blood pressure was measured after 5 min rest, with participants seated, using an Omron HEM 705-CP automated sphygmomanometer (Omron Healthcare Inc., Bannockburn, IL) and an appropriate sized cuff. Two measurements were obtained with the average value used in analyses.
Blood samples were obtained after an overnight fast for plasma glucose, insulin, cortisol and lipids. The fasting sample was obtained at 0830 h, and in the first half of the menstrual cycle in females, in order to limit variability in plasma cortisol levels. Following the fasting sample, participants underwent a standard 75 g oral glucose tolerance test, with glucose and insulin levels measured at 30 and 120 min, respectively.
The Auckland Regional Ethics Committee approved the study on behalf of all New Zealand Regional Ethics Committees. Written informed consent was obtained from each participant.
Statistical analysis
The aim of the analysis in this article was to measure any independent influence of gestational age and fetal growth, explored as birth weight z-scores, on systolic blood pressure, fasting plasma cholesterol, fasting plasma triglyceride, fasting plasma cortisol and measures of insulin and glucose following a standard 75 g oral glucose tolerance. The three glucose and insulin measures were combined to give a composite insulin measure and a composite glucose measure of area under the curve. Plasma cortisol, triglyceride and insulin values were log-transformed in order to preserve the assumption of normality for the regression. Birth weight z-scores were created using data from all New Zealand deliveries in 1990–91.15 New Zealand Socio-economic Index scores were assigned from occupational data.16
Analyses were performed using SAS version 8.02 (SAS Institute, Cary, NC) and S-Plus version 6.1 (Insightful Corporation, Seattle). Multiple linear regression was used to assess the relationship between both gestational age and birth weight and adult outcomes. The effect of pre-term birth was also investigated as a binary variable in the regression models, defined as birth before 37 completed weeks gestation. The effect of birth weight, independent of pre-term birth, was investigated using birth weight z-scores, as these are adjusted for gestational age and are thus independent of pre-term birth. Results are presented as the regression coefficient (β) ± the standard error (SE). Results are initially for univariate analysis. Further multivariate analysis included adjustment for sex, antenatal betamethasone exposure and current body mass index decided a priori. In addition, in the univariate and multivariate analyses of the effect of gestational age and pre-term birth, adjustment for birth weight z-scores was included.
Further exploratory analyses were conducted to determine the shape of the association between gestational age and significant outcomes, following multiple linear regression, using generalized additive models (spline regression).
Background characteristics of the cohort were compared using standard tests. Continuous variables were compared with unpaired t-tests or Mann–Whitney tests for parametric and non-parametric data, respectively. Categorical data were compared with 
2 tests. Data are presented as means ± standard deviation (SD), medians [interquartile range (IQR)], or number (percentage).
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Results |
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Recruitment and background perinatal characteristics
Of the 988 neonatal survivors, 713 (72%) were successfully traced. Five hundred and thirty-four participants were subsequently enrolled in the 30-year follow-up (56% of those presumed to be alive and 80% of those traced and presumed to be alive).
Twenty-seven (4%) participants (n = 639) who had been born pre-term and 15 (4%) who had been born at term (n = 349) died between 28 days of age and the 30-year follow-up [relative risk (RR) = 0.98, 95% CI 0.53–1.82, P = 0.98]. The median age at death was earlier in those born pre-term [pre-term = 0.3 years (IQR = 0.2–5.3), term = 18.4 years (IQR = 0.4–21.8), P = 0.006]. There was no difference in the primary cause of death between those born pre-term and those born at term.
Of the 534 participants who completed the 30-year follow-up, 458 (86%) had data on the primary outcomes of interest in this study. One hundred and forty-seven participants had been born at term and 311 participants had been born pre-term (this represents 51% of all survivors born at term and 44% of survivors born pre-term who were presumed to be alive at age 30, P = 0.05). Those with follow-up at age 30 were more likely to be from a multiple pregnancy, female and born pre-term compared with those presumed to be alive but without follow-up.12 Those who participated were also lighter at birth. This difference was due to being born at an earlier gestational age, as both groups had similar birth weight z-scores. There were no significant differences in other perinatal characteristics between those with follow-up and those presumed to be alive but without follow-up (Table 1).
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Of the participants with follow-up, those who had been born pre-term were more likely to be from a multiple pregnancy, a pregnancy complicated by hypertension syndromes, haemolytic disease or an instrumental delivery. The median gestational age at delivery was 34 weeks and 1 day in the pre-term group and 39 weeks and 4 days in the term group. Participants who were born pre-term had higher rates of low Apgar scores and respiratory distress syndrome compared with participants born at term. There was no difference in exposure to antenatal betamethasone between participants born pre-term and those born at term (Table 2). Participants born pre-term were less likely to have a maternal family history of coronary heart disease compared with those born at term [pre-term = 22 (7%), term = 22 (15%), P = 0.008]. Adjustment for this did not change any of the results.
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Adult follow-up
Participants born pre-term were less likely to use tobacco or illicit drugs than those born at term. There was no difference in alcohol use, marital status, education attainment, exercise or socio-economic status between those born pre-term and those born at term (Table 3).
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No participant born pre-term and one (1%) born at term had a history of ischaemic heart disease. One (0%) participant born pre-term and one (1%) born at term had a history of cerebrovascular disease. There were no differences in rates of antihypertensive medication or oral contraceptive use between the two groups (Table 3).
A previous diagnosis of hypertension was reported by 61 (20%) participants born pre-term and 14 (10%) born at term (RR = 2.1, 95% CI 1.2–3.6, P = 0.01). This effect was still present after excluding hypertension associated with pregnancy [non-pregnancy related hypertension in pre-term = 34 (11%), term = 3 (2%), RR = 5.4, 95% CI 1.7–17.2, P < 0.001]. Both a lower gestational age at birth and being born pre-term were associated with higher systolic blood pressure at age 30 (Table 4). For example, systolic blood pressure at age 30 increased by 0.5 mmHg for each week decrease in gestational age at birth in the univariate model (P = 0.006). Similarly, being born pre-term increased systolic blood pressure by 3.5 mmHg at age 30 (P = 0.009). Adjustment for sex, antenatal betamethasone exposure, birth weight z-scores and current BMI did not change the results. However, assessment of the association between gestational age and later systolic blood pressure using generalized additive techniques suggests that the shape of this association is not consistent across the range of gestational ages studied (P-value for linearity in adjusted spline regression = 0.002, Figure 1). Lower birth weight was also associated with increased systolic blood pressure at age 30, with an increase of 1.6 mmHg for each kilogram decrease in birth weight in the adjusted model (P = 0.03). However, this relationship was abolished after further adjustment for pre-term birth by using birth weight z-score analysis, indicating that fetal growth independent of gestational age is not associated with systolic blood pressure at age 30 (Table 4). Exclusion of participants taking antihypertensive medication or from pregnancies complicated by hypertension did not alter the results.
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A previous diagnosis of hyperlipidaemia was reported by 24 (8%) participants born pre-term and 11 (7%) born at term (RR = 1.0, 95% CI 0.52–2.0, P = 0.93). There was no association between gestational age, pre-term birth or birth weight and fasting plasma cholesterol or triglyceride levels at age 30 (Table 4).
There was no association between gestational age, pre-term birth or birth weight and fasting plasma cortisol levels at age 30 (Table 4).
There was no association and there was also no association between gestational age, or pre-term birth and fasting plasma insulin levels at age 30 (Table 4). However, following the 75 g oral glucose load, both a lower gestational age at birth and being born pre-term were associated with increased insulin area under the curve, in both univariate and adjusted models (Table 4). Assessment of the association between gestational age and plasma insulin levels following a glucose tolerance test using generalized additive techniques suggests that the shape of this association was consistent across the range of gestational ages studied (P-value for linearity in spline regression of insulin area under curve = 0.42, Figure. 1). Birth weight was negatively associated with fasting and 120-min insulin levels and insulin area under the curve in the adjusted model. This association was weakened or abolished when gestational age was taken into account in the birth weight z-score analysis (Table 4).
There was no association between gestational age, or pre-term birth and either fasting glucose levels or glucose levels following a 75 g oral glucose load at age 30 (Table 4).
There was a weak negative association between birth weight and 120-min glucose levels in the adjusted model. This association was abolished in the birth weight z-score analysis. Birth weight z-score was positively associated with 30-min glucose levels at age 30 following an oral glucose load. However, this association was abolished after adjustment for sex, antenatal betamethasone exposure and current BMI (Table 4).
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Discussion |
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We studied a cohort of 458 neonatal survivors at 30 years of age whose mothers had participated in a randomized controlled trial in the perinatal period.10,11 We found no association between gestational age at birth, pre-term birth or birth weight, independent of gestational age, with fasting plasma cholesterol, triglyceride or cortisol levels. However, a low gestational age at birth, and pre-term birth, were associated with increased adult systolic blood pressure and insulin resistance. Birth weight, independent of gestational age, was not associated with adult systolic blood pressure and insulin resistance. These data suggest that length of gestation, rather than fetal growth, may be a major contributor to the relationship between size at birth and cardiovascular risk in adulthood.
In the initial epidemiological studies detailing a relationship between size at birth and later risk of disease, data were not available concerning gestational age.2 It is likely that a number of participants with low birth weight in those studies were indeed born mildly pre-term. Those studies that did have data on length of gestation either included very few pre-term infants or excluded such infants.3–6,17 Thus, there has been little information to date concerning the independent contributions of fetal growth and length of gestation to birth weight in relation to later outcomes.
Two other small studies have reported an association between pre-term birth and altered insulin levels. In 61 individuals at age 24, pre-term birth was associated with increased fasting insulin levels,18 but the authors were unable to demonstrate whether gestational age or birth weight was the more important influence on outcome.19 Similarly, pre-term birth was associated with later increased insulin resistance, though not fasting insulin levels, in 72 pre-pubertal children.20 In our much larger study, we also found that lower gestational age and pre-term birth were associated with insulin resistance, as indicated by increased 30-min and 120-min insulin levels, and insulin area under the curve in response to an oral glucose challenge, though not with fasting insulin levels. Furthermore, the relationship between gestational age and later insulin levels was similar across the range of gestations studied in our cohort, suggesting a graded effect and that even mild degrees of prematurity may be associated with altered glucose/insulin axis function in adulthood. In our study, birth weight adjusted for gestational age was not associated with evidence of later insulin resistance. Thus gestational age, hence pre-term birth, appears to be the more important influence on later insulin resistance.
Similarly, gestational age, hence pre-term birth, appears to be the more important influence on later systolic blood pressure. Indeed, even at the relatively young age of 30 we found twice as many participants with diagnosed hypertension amongst ex-pre-term infants, despite the fact that this group were born only moderately pre-term [62 (20%) of the pre-term group born at <32 weeks gestation]. Doyle et al. reported higher systolic blood pressure at age 18 in a cohort of 156 individuals who had been born at <1501 g.21 As in our study, the authors assessed the effect of poor fetal growth by using birth weight z-scores, and concluded that this did not influence later blood pressure. Irving et al.18 also reported increased systolic blood pressure in their cohort of ex-pre-term infants at age 24. The long-term effect of such increased blood pressure into later life remains unknown. However, there is considerable concern given that those whose blood pressure is in the highest quintile in their 20s and 30s are more than twice as likely to remain in that quartile in later life, at the time of peak cardiovascular incidence.22
Despite the known problems of unstable estimates at the tails with generalized additive modelling23 the shape of the relationship found between gestational age and later systolic blood pressure using this method is intriguing. The results appear to suggest a different relationship between gestation and blood pressure amongst those born at <35 weeks compared with those born at term. At 35 weeks, gestational age appears to be negatively (non-linearly) associated with blood pressure, while at term the association between gestational age and blood pressure appears linear. This interpretation is consistent with the findings of Siewert-Delle and Ljungman24 who have examined the impact of birth weight and gestational age on later blood pressure in a cohort of 430 Swedish men at age 49. They reported that adult systolic blood pressure was inversely correlated with gestational age (r = –0.10, P = 0.04). This correlation was stronger in the small number of pre-term subjects [n = 44 (10%), r = –0.46, P = 0.001]. However, as suggested by Figure 1, there was no correlation between adult systolic blood pressure and gestational age in subjects born at term or post-term. In contrast, in a much larger population study of 329 495 male Swedish Military Conscripts at age 18, Johansson et al.25 found a consistent negative association between blood pressure and gestational age at birth, including individuals born at 24–28 weeks gestation.
Alterations to the HPA axis have been proposed as a mechanism to explain the epidemiological link between low birth weight and later increased blood pressure.26 Low birth weight has been associated with increased adult cortisol levels in three populations.5 However, these studies have focused on populations born at term. Reports from pre-term populations have been contradictory. A study of 100 individuals at age 24 reported increased serum cortisol levels in both appropriate- and small-for-gestational-age ex-pre-term infants.27 Conversely, Irving and colleagues reported no difference in plasma cortisol levels in both male and female ex-pre-term infants, but lower urinary cortisol secretion in the subset of ex-appropriate-for-gestational-age females.28 In our much larger study, plasma cortisol levels were not associated with gestational age, pre-term birth or birth weight, independent of gestational age.
Previous studies in childhood29 and adulthood18 have not found an association between gestational age or pre-term birth and total plasma cholesterol or triglyceride levels, although being born pre-term has been associated with abnormalities of cholesterol synthesis and breakdown.29 Clinicians should be reassured that despite the subtle changes documented in childhood there appear to be no differences between term and mildly pre-term babies in measured total plasma cholesterol or triglyceride levels at age 30.
The Auckland Steroid Trial is particularly well suited to reporting the long-term effects of pre-term birth. Administration of antenatal glucocorticoids was one of the first treatments to significantly decrease mortality and morbidity in infants born pre-term.9,30 Thus, survivors of the original trial represent one of the oldest cohorts of ex-pre-term infants available. The findings are particularly relevant as the majority of infants born pre-term each year experiences only the moderate levels of prematurity found in this cohort.7 Furthermore, the trial has a distinct advantage over retrospective studies as information on gestational age, birth weight and perinatal outcomes was collected prospectively. In addition, individuals born at term in this cohort may reflect a better control population to test the true effect of pre-term birth compared with case control studies matched after birth, as all participants, whether born pre-term or at term, were exposed to the risk of pre-term birth. Ultimately though the ideal study is a large prospective cohort of all pregnancies that is sufficiently powered to examine the effect of threatened and actual pre-term birth.
There are a number of limitations to our study. Follow-up was obtained for 56% of those presumed to be alive. However, lack of complete follow-up would only bias our results if the association between pre-term birth and cardiovascular risk differed between those who did and did not participate. Since those who participated in the study had few differences in maternal, neonatal and adult characteristics from those who were eligible but who did not participate, there is no reason to think this might be the case. Furthermore, participants were asked to enter a follow-up study of antenatal betamethasone treatment and were not aware of the potential for this analysis based on pre-term birth.
There is further potential for bias due to clustering of outcomes in siblings from multiple pregnancies. However, analysis of just those participants from singleton pregnancies did not change the results.
In addition, the findings of our study should be interpreted in light of the multiple comparisons undertaken in the analysis. However, many of the associations were statistically extreme and so would still be apparent using more conservative P-value thresholds.
Finally, size at birth is a poor surrogate for fetal compromise or an adverse fetal environment, and it has been proposed that it is the adverse fetal environment that lies on the causal pathway to risk of later adult disease. Small size at birth may or may not be an endpoint of the same adverse fetal environment. However, small size at birth (birth weight or birth weight z-scores) remains a convenient way in man to explore relationships between adverse fetal environments and later disease risk. Our birth weight z-scores were derived from all deliveries in New Zealand in 1990–91,15 primarily due to the increased precision of pre-term birth weights available in this data set. Since mean birth weights increased between the 1970s and the 1990s,15 the birth weight z-scores calculated for this cohort are lower than they would have been if a contemporaneous data set had been used. Ultrasonography studies also suggest that birth weight z-scores may underestimate the number of growth-restricted fetuses at any given pre-term gestation. However, exclusion of infants defined as small for gestational age (birth weight <10th centile) did not change the overall results. This is consistent with previous reports that the relationships between size at birth and later disease risk apply across the range of birth weights rather than being confined to the extremes.
It is not possible from the results of our study to determine whether pre-term birth lies on the causal pathway for later disease risk or is merely another marker for an adverse fetal environment. Pre-term birth exposes an individual to nutritional, metabolic, hormonal, sensory and respiratory environments that are all very different to those experienced in utero, and these environmental factors themselves may alter development of physiological systems in ways that predispose to later disease risk.17 Pre-term birth also results in earlier maturation of a number of organ systems, and the long-term consequences of earlier maturation are still unknown. However, pre-term birth is also commonly associated with maternal disease, poor placental function or fetal disease. Both periconceptional undernutrition in sheep,31 and low pre-pregnancy maternal weight or history of eating disorders in women,32 are associated with pre-term birth. Thus gestation length may merely provide another surrogate marker, perhaps neither more nor less direct than size at birth, for various aspects of the intrauterine environment, which are causal in determining later disease risk.
We conclude that adults who were been born moderately pre-term have increased blood pressure and insulin resistance at 30 years of age. Pre-term birth rather than poor fetal growth is the major determinant of this. As the proportion of pre-term births is increasing, and increasing numbers of pre-term infants are now surviving into adulthood, it is likely that ex-pre-term survivors will contribute an increasing proportion of the overall burden of cardiovascular disease in developed countries.
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We are indebted to the mothers and their children for participation in the original Auckland Steroid Trial and the Steroid Follow-up Study. We thank Associate Professor Ross Howie and Professor Mont Liggins for making the Auckland Steroid Trial data available. We also thank Ms Mary Wills for study management; Ms Sue Hawkins and Ms Maria Harrison for data collection; Dr Natalie Walker, Professor Colin Mantell and Professor Harry Rea for their involvement in the Steroid Follow-up Study and Dr John Thompson for making data available to create birth weight z-scores. Funding was obtained from: Health Research Council of New Zealand, Auckland, New Zealand; Auckland Medical Research Foundation, Auckland, New Zealand and New Zealand Lottery Grants Board, Wellington, New Zealand.
Conflict of Interest: None declared.
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  R. Pyhala, K. Raikkonen, K. Feldt, S. Andersson, P. Hovi, J. G. Eriksson, A.-L. Jarvenpaa, and E. Kajantie Blood Pressure Responses to Psychosocial Stress in Young Adults With Very Low Birth Weight: Helsinki Study of Very Low Birth Weight Adults Pediatrics, February 1, 2009; 123(2): 731 - 734. [Abstract] [Full Text] [PDF]
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 R. Cooper, K. Atherton, and C. Power Gestational age and risk factors for cardiovascular disease: evidence from the 1958 British birth cohort followed to mid-life Int. J. Epidemiol., February 1, 2009; 38(1): 235 - 244. [Abstract] [Full Text] [PDF]
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F. Mardones, L. Villarroel, L. Karzulovic, S. Barja, P. Arnaiz, M. Taibo, and F. Mardones-Restat Association of perinatal factors and obesity in 6- to 8-year-old Chilean children Int. J. Epidemiol., August 1, 2008; 37(4): 902 - 910. [Abstract] [Full Text] [PDF]
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E. Kajantie, P. Hovi, K. Raikkonen, A.-K. Pesonen, K. Heinonen, A.-L. Jarvenpaa, J. G Eriksson, S. Strang-Karlsson, and S. Andersson Young Adults With Very Low Birth Weight: Leaving the Parental Home and Sexual Relationships--Helsinki Study of Very Low Birth Weight Adults Pediatrics, July 1, 2008; 122(1): e62 - e72. [Abstract] [Full Text] [PDF]
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