Published online before print November 21, 2005, doi: 10.1161/CIRCULATIONAHA.105.540906
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2005;112:3430-3436.)
© 2005 American Heart Association, Inc.
Hypertension |
Risk of High Blood Pressure Among Young Men Increases With the Degree of Immaturity at Birth
From the Departments of Medical Epidemiology and Biostatistics (S.J., A.I., N.B., S.C.) and of Woman and Child Health (S.J., M.N.), and the Clinical Epidemiology Unit (A.I.), Department of Medicine, Karolinska Institute, Stockholm, and the Department of Women’s and Children’s Health (T.T.), Uppsala University, Uppsala, Sweden.
Correspondence to Stefan Johansson, Department of Medical Epidemiology and Biostatistics, Karolinska Institute, PO Box 281, SE-171 77 Stockholm, Sweden. E-mail stefan.johansson{at}ki.se
Received February 5, 2005; revision received September 13, 2005; accepted September 27, 2005.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background— Survivors of preterm birth constitute a new generation of young adults, but little is known about their long-term health. We investigated the association between gestational age (GA) and risk of high blood pressure (HBP) in young Swedish men and whether GA modified the risk of HBP; ie, whether HBP was related to being born small for gestational age (SGA).
Methods and Results— This population-based cohort study included 329 495 Swedish men born in 1973 to 1981 who were conscripted for military service in 1993 to 2001. Multivariate linear- and logistic-regression analyses were performed. Main outcome measures were systolic and diastolic BPs at conscription. Linear-regression analyses showed that systolic BP increased with decreasing GA (regression coefficient –0.31 mm Hg/wk, P<0.001). Systolic and diastolic BPs both increased with decreasing birth weight for GA, but the association with systolic BP was most evident (regression coefficient –0.67 mm Hg per SD score in birth weight for GA, P<0.001). Compared with men born at term (GA, 37 to 41 weeks), the adjusted odd ratios (95% confidence intervals [CIs]) for high systolic BP (
140 mm Hg) were as follows: moderately preterm (33 to 36 weeks), 1.25 (1.19 to 1.30); very preterm (29 to 32 weeks), 1.48 (1.30 to 1.68); and extremely preterm (24 to 28 weeks), 1.93 (1.34 to 2.76). Being SGA was associated only with an increased risk of high systolic BP among men born at 33 weeks or later. The risk estimates for high diastolic BP (90 mm Hg) increased with decreasing GA, but the risk reached significance only among men born moderately preterm.
Conclusions— Preterm birth, a common pregnancy complication, is a risk factor for HBP in young men. The risk of high systolic BP associated with birth weight for GA is modified by GA, suggesting that perinatal contributions to BP elevation later in life may be induced by different biological pathways.
Key Words: infant • premature birth • blood pressure • epidemiology • adult
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The development of neonatal intensive care during recent decades has led to improved survival rates among preterm infants. However, the life-long health effects after very or extremely preterm birth are virtually unknown, and late morbidity could be an increasing problem. Low birth weight is related to the unfavorable constellation of high blood pressure (HBP), glucose intolerance, and hyperlipidemia later in life, predisposing low-birth-weight infants to increased mortality in coronary heart disease and stroke.1 It has been suggested that the association between low birth weight and the risk of cardiovascular disease is mediated by fetal growth restriction in term birth rather than preterm birth.2 However, that study was based on a birth cohort from the early 20th century, when mortality rates among preterm infants were very high. Today, the most common cause of low birth weight in most countries is preterm birth.3
Although a developmental origin for cardiovascular disease is a well-supported hypothesis, methodological weaknesses, including publication bias and inappropriate adjustment for current weight, may have led to overestimation of the association between birth weight and BP later in life.4 Moreover, the independent effects of low birth weight due to preterm birth or fetal growth restriction and the possible influence of childhood growth have not been fully elucidated. Preterm birth may attenuate the association between being born small for gestational age (SGA) and the risk of HBP,5,6 and GA may modify the association between body mass index (BMI) in adulthood and BP.7 In addition, accelerated weight gain in childhood may itself be a risk factor for BP elevation later in life.7,8
In small clinical studies, adolescents and young adults born very preterm have structural changes in the vascular tree9,10 and higher systolic BPs (SBPs)5,6,10,11 than individuals born at term. Results from Swedish population-based cohort studies suggest that GA may be inversely associated with BP.12–14 However, the strength of the association has not been studied among survivors of very short gestations, and one of the previous studies did not include individuals with GAs <35 weeks.13 Moreover, those studies did not account for genetic and socioeconomic factors, which may influence both GA15,16 and the risks for cardiovascular diseases.17,18 Finally, intrauterine growth restriction is overrepresented among preterm births,19 emphasizing the importance of using reference curves based on fetal growth rather than recorded birth weights when assessing the relation between birth weight for GA and later BP.
We hypothesized that the risk of HBP in young men increases with the degree of immaturity at birth, independent of socioeconomic and familial factors. In addition, we wanted to explore interactions between GA, birth weight for GA, and BMI in young adulthood with regard to the risk for HBP.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Design and Population
This cohort study was based on 4 population-based Swedish registers: the Medical Birth Register, the Conscript Register, the Multigeneration Register, and the Population and Housing Census 1990. The national registration number, assigned to each Swedish resident at birth, was used for individual record linkage.
The Medical Birth Register contains data on >99% of all births in Sweden since 1973. Starting at the first prenatal visit, information is prospectively collected on standardized records and forwarded to the registry. Mortality data are added through linkage to the Cause of Death Register. The Medical Birth Register has recently been validated, and the quality of the variables included in the present investigation is considered high.20
The Conscript Register contains information about young men assessed for military service. Conscription is mandatory and is enforced by law, but men with severe handicaps or congenital malformations generally receive an exemption. Conscription starts with an interview, including questions about health, followed by an IQ test. Men with acceptable cognitive function and a good physical history undergo a physical examination, including BP measurements.
The Multigeneration Register includes information about first-degree relatives for Swedish residents and was used to identify full brothers within the study population.
In the Population and Housing Census 1990, data on individuals and families were collected by postal enquiries, including information on socioeconomic characteristics such as education, profession, and housing. Participation was mandatory for all residents in Sweden with an age of 16 years and older. The response rate was 97.5%.21
From 1973 to 1981, there were 458 371 male live births recorded in the Medical Birth Register. To increase the homogeneity of the study population, we excluded multiple births, congenital malformations, infants to non-Nordic mothers, and those who died before 18 years of age (n=54 649). Thus, the study population included 404 306 men, of whom 379 963 (94%) were conscripted between 1991 and 2001. In our analyses, we excluded men with no recorded GA and men with a recorded GA of <24 weeks or >43 weeks (n=4217). Information on SBP was available for 329 495 (82%) men, and information on diastolic BP (DBP) was available for 328 109 (82%) men. The proportion of men with recorded (systolic and diastolic) BP values increased with GA, as follows: 24 to 28 weeks, 63%; 29 to 32 weeks, 74%; 33 to 36 weeks, 80%; 37 to 41 weeks, 82%; and 42 to 43 weeks, 83%. Among men born extremely preterm (24 to 28 weeks), those who did not complete conscription had a lower mean GA compared with those who completed conscription (26.9 versus 27.4 weeks, P<0.05). Corresponding differences among men born after week 28 were minor or none (data available on request).
Variables
Information about GA, birth weight, maternal age, and parity was obtained from the Medical Birth Register. During the study period, GA was estimated from the date of the last menstrual period. The GA distribution was scrutinized according to the method described by Alexander et al,22 and erroneous values were considered missing (n=211). GA was classified as extremely preterm (24 to 28 completed gestational weeks), very preterm (29 to 32 weeks), moderately preterm (33 to 36 weeks), term (37 to 41 weeks), and postterm (42 to 43 weeks). The classification of extremely preterm birth was introduced to include a sufficient number of individuals for statistical analyses. Birth weight for GA was classified as small, appropriate, and large for gestational age (SGA, AGA, and LGA, respectively), according to the Swedish reference curve for normal fetal growth.19 The reference curve defines SGA and LGA as a birth weight >2 SDs below and above the mean reference weight for GA, respectively. Birth weights for GA >5 SDs above or below the mean were judged implausible and hence, considered missing (n=46). Maternal age and parity were recorded at delivery.
At the time of military conscription, weight was measured in kilograms and height in centimeters. BP was measured under standardized circumstances according to written instructions (Dr Wågermark, National Service Administration, Stockholm, Sweden; personal communication, 2005). After the subjects rested for 5 to 10 minutes in the supine position, nurses assigned for fitness testing measured the BP in the right arm. BP was determined from the appearance (Korotkoff sound phase 1) and disappearance (Korotkoff sound phase 5) of pulsations auscultated over the brachial artery. Before 1998, different cuffs were used for different diameters of the upper arm, but from 1998, the so-called Tri-cuff device was introduced. The Tri-cuff has 3 air chambers, and the width of the air chamber depends on the diameter of the arm. When BP was considered elevated (SBP 135 mm Hg or DBP 85 mm Hg), a second measurement was performed, and the lower measurement was recorded. High SBP was defined as 140 mm Hg, and high DBP was defined as 90 mm Hg.23 BMI at conscription was calculated as weight divided by the square of height (kg/m2). Low weight was defined as a BMI 
18.4 kg/m2, normal weight as a BMI 18.5 to 24.9 kg/m2, overweight as a BMI 25.0 to 29.9 kg/m2, and obesity as a BMI 30 kg/m2, as suggested by the World Health Organization.24
Information about parental socioeconomic and educational status and family structure was obtained from the Population and Housing Census 1990. We defined each household’s socioeconomic status as the highest socioeconomic status in the family, and the household’s educational status was defined analogously. Family structure was defined as living with both parents, living with a single parent, or with living foster parents. The study was approved by the research ethics committee at Karolinska Institute.
Statistical Analysis
We estimated odds ratios (OR) and 95% confidence intervals (CIs) according to the GENMOD procedure in version 8 of the SAS software package (SAS Institute, Inc). Interactions were tested with the same procedure, and a probability value for the overall effect is given. The outcome variables were SBP and DBP. Covariates in the analyses were categorized and included GA, birth weight for GA, maternal age, parity, BMI and height at conscription, conscription year, family structure of the conscriptor, and parents’ educational and socioeconomic status. Conscription year was added to the model to control for possible cohort effects. Using linear-regression analyses, we also calculated regression coefficients with SEs per 1-week change in GA, per 1-unit change in SD score in birth weight for GA, and per 1-unit change in BMI. We corrected for clustering effects between brothers in the cohort according to the generalized estimating equation method. Because BMI could be an intermediate variable in a possible causal chain between birth characteristics and risk of HBP, we analyzed our data with and without BMI as a covariate in the multivariate-regression models.
We assessed whether an association between GA and HBP was confounded by familial factors by performing analyses between and within families. Familial effects on the risk of HBP include shared genetic and environmental factors. The analyses were restricted to males with at least 1 full brother in the cohort (n=106 576). In analyses of familial effects on an association between exposure and outcome, the exposure was decomposed into between- and within-family components. The between-family component was measured by the family mean of the exposure measurement (Xi, where i=family number), and the within-family component was measured by the individual deviation from the family mean (Xij–Xi, where i=family number and j=individual in family i). If familial factors are important, they tend to make family members more alike. Hence, the within-family component would be nonsignificant, whereas the between-family component would be significant. If the within-family component remains significant, this indicates that the association between exposure and outcome depends on other than familial factors. Our between-family component estimated the change in risk of HBP per 1–gestational week decrease in the family mean. Our within-family component estimated the change in the risk of HBP per 1–gestational week difference from their family mean.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The characteristics of the conscripted men are presented in Table 1. Multivariate linear-regression analyses showed that SBP increased with decreasing GA, decreasing birth weight for GA, and increasing BMI (Table 2). DBP also increased with decreasing birth weight for GA and increasing BMI, but there was no linear association with GA.
|
|
A large proportion (20%) of the conscripted men were assessed as having a high SBP (140 mm Hg). The proportion of men with a high SBP varied from 32% among men born extremely preterm (28 weeks) to 19% among men born postterm (42 weeks; Table 3). The risk of high SBP consistently increased with decreasing GA. Compared with men born at term (37 to 41 weeks), men born extremely preterm faced an almost 2-fold increased risk of high SBP (Table 3). Being born SGA was associated with a 10% increased risk of high SBP compared with being born AGA.
|
A small proportion (0.6%) of the conscripted men were assessed as having a high DBP (90 mm Hg). The proportion of men with a high DBP varied from 1.2% among men born extremely preterm (28 weeks) to 0.6% among men born postterm (42 weeks; Table 3). The risk of high DBP increased with decreasing GA, but only men born moderately preterm (33 to 36 weeks) had a significantly increased risk of high DBP (Table 3). Being born SGA was not associated with risk for high DBP in the logistic-regression analyses.
The risk estimates for high SBP related to GA and birth weight for GA did not essentially change when BMI was included as a covariate in the regression models (Table 3). Compared with men with a normal BMI at conscription, obese men faced a 2-fold increase in risk of high SBP and a 3-fold increase in risk of high DBP.
To further explore the association between GA and the risk of HBP, analyses were repeated with regard to an SBP of 145 mm Hg (prevalence, 4.5%) and a DBP of 85 mm Hg (prevalence, 2.3%). Compared with men born at term, the adjusted ORs (95% CIs) with regard to an SBP of 145 mm Hg were as follows: moderately preterm (33 to 36 weeks), 1.44 (1.34 to 1.56); very preterm (29 to 32 weeks), 2.09 (1.71 to 2.55); and extremely preterm (24 to 28 weeks), 2.72 (1.58 to 4.70). With regard to a DBP of 85 mm Hg, men born moderately and very preterm faced significantly increased risks. Compared with men born at term, the adjusted ORs (95% CIs) were as follows: moderately preterm (33 to 36 weeks), 1.25 (1.11 to 1.40); very preterm (29 to 32 weeks), 1.53 (1.12 to 2.09); and extremely preterm (24 to 28 weeks), 1.84 (0.80 to 4.20).
The risk of a high SBP (140 mm Hg) per 1-week decrease in GA increased both within and between families (adjusted ORs [95% CIs] were 1.03 [1.01 to 1.05] and 1.06 [1.04 to 1.08], respectively), indicating that an association between GA and SBP exists after controlling for common genetic and shared environmental factors after birth. Analyses for within and between families with regard to high DBP (90 mm Hg) were not possible because of the small numbers of very preterm–born men with a high DBP.
There was a significant interaction between GA and birth weight for GA (P=0.03) with regard to high SBP (140 mm Hg). To enable stratified analyses by GA, we collapsed extremely and very preterm births into 1 category (32 weeks). SGA was not a risk factor for high SBP among men born at 24 to 32 gestational weeks but increased the risk of high SBP among men with longer gestations (Table 4). We found no significant interactions between GA and BMI at conscription (P=0.16) or between birth weight for GA and BMI at conscription (P=0.23). Interaction analyses with regard to high DBP (90 mm Hg) were not possible because of the small numbers of very preterm–born men with high DBP.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
In today’s generation of young Swedish men, preterm birth was identified as a perinatal risk factor for high SBP, and the risk increased with decreasing GA. SGA was also associated with an increased risk for high SBP but only among men born at 33 weeks or later. SGA and preterm birth represent different clinical entities, and their relative contributions to high SBP are not easily compared.
Analyses of DBP showed less consistency. Decreasing birth weight for GA was associated with increasing DBP in linear-regression analyses, whereas logistic-regression analyses showed no association between SGA and the risk of high DBP. The latter finding could be due to the low prevalence of high DBP in the study cohort. SGA may also be less expressive for the risk of high DBP compared with the risk of high SBP. No linear association was found between GA and DBP. However, the risk of high DBP increased consistently with decreasing GA, although only men born moderately preterm (33 to 36 weeks) faced a significantly increased risk. This discrepancy may be due to a nonlinear relation between GA and DBP.
Individuals born preterm may be prone to BP elevation through several mechanisms. Abnormal vascular growth and development induced by preterm birth may contribute to increased vascular resistance.9,10 Autonomic BP regulation is immature in very preterm infants, and the postnatal maturation of this homeostatic control mechanism differs from that seen in infants born at term.25 Very-preterm infants commonly suffer from metabolic problems such as transient hyperglycemia despite relatively high levels of insulin.26 Increased postnatal levels of insulin may cause persisting changes in glucose and lipid metabolism, predisposing to increased BP later in life.27 Activation of the hypothalamic-pituitary-adrenal axis has been suggested to link low birth weight at term to high SBP in adulthood.28 The immature hypothalamic-pituitary-adrenal axis in preterm infants29 and the possibility of early programming of the numbers of glucocorticoid receptors30 may be important for the association between preterm birth and HBP later in life. Finally, a reduction in nephron number cannot be ruled out as another etiologic factor, but at least women born preterm exhibit HBP despite normal kidney function.11
Whereas preterm birth per se may be conditional for the risk of HBP later in life, postnatal environmental exposures are likely to have an impact as well. In a randomized, controlled trial, preterm infants fed breast milk had lower BPs at follow-up in adolescence compared with those receiving formula.31 In addition, postnatal nutrient intake and growth patterns have been associated with insulin resistance32 and with vascular endothelial function in infancy33 and later in life.34 The full nature of these associations needs to be clarified, but they indicate that the risk for HBP in adults born preterm could be already modulated in the neonatal nursery.
SGA was not a risk factor for BP elevation among men born very preterm, and similar conclusions have been drawn in smaller clinical studies.5,6 One may argue that the strong effect of very-preterm birth could mask a smaller effect of being SGA. However, there may also be principally different pathways of inducing later BP elevation in individuals born preterm and term. For example, dysfunction of the vascular endothelium, causing impaired vascular relaxation, has been found in infants and children born SGA at term, whereas very-preterm infants had normal endothelial function regardless of birth weight for GA.33,34
We did not find any interaction between GA and BMI in adulthood, which is in contrast to results from a recent study.7 Differences in study populations may contribute to this discrepancy, including different distributions of GA and differences in age when BP was measured. Because accelerated weight gain in childhood has been reported to influence the risk of HBP,8 we were somewhat surprised that there was no interaction between birth weight for GA and BMI at conscription. However, we had no longitudinal information on weight and height during childhood and adolescence, and negative findings for these 2 interaction analyses should be interpreted cautiously.
Our study was based on a national cohort of individuals born when neonatal intensive care was developing rapidly and survival rates for preterm infants were increasing. We used a reference curve for normal fetal growth instead of a reference curve based on birth weight and could therefore apply a more accurate definition of SGA in our cohort. Data for the main exposures (GA and birth weight) were registered prospectively. All analyses were adjusted for perinatal, maternal, and socioeconomic factors. In addition, the associations between GA and risks of high SBP were similar among men from different families and within families of full brothers. Thus, it is unlikely that the risk of high SBP related to short GA was confounded by common genetic and shared environmental factors in childhood.
Our cohort included only men, and conclusions should be restricted to men. GA was determined by the last menstrual period, which may slightly underestimate GA35 and hence, the effect of preterm birth on the risk of HBP. Conscription rates varied across the GA range, with the lowest conscription rate among men born extremely preterm. Because conscripted men probably are healthier than those not conscripted, this potential selection bias would, if anything, underestimate the effect of preterm birth. We had no information about maternal smoking and preeclampsia, which are associated with risks of preterm birth16,36 and may also influence their offspring’s risk of HBP.37,38
Despite standardized circumstances for the physical assessment of BP at conscription in Sweden, validation studies are lacking. In addition to the usual problems of BP measurement, it is reasonable to believe that young men experience some stress and hence, a moderate BP elevation, during military conscription similar to so-called "white coat hypertension." Because a differential misclassification of SBP elevation (140 mm Hg) between individuals with different GAs or birth weights is unlikely, such limitations would, if anything, only attenuate our results. When we repeated our analyses with a narrower definition of high SBP (145 mm Hg), the association between preterm birth and risk of high SBP became even stronger. Similarly, the strong association between preterm birth and high DBP, when defined as 85 mm Hg, also lends support to the hypothesis that preterm birth predispose to BP elevation later in life.
The strong effect of preterm birth on later BP may have important public health implications, because BP elevation could lead to hypertension with time.23 In Sweden, &6% of pregnancies end preterm, and the corresponding figure in the United States is reported to be as high as 12%.3 Hence, a similarly large proportion of offspring could be at risk for increased BP later in life. A proposed strategy to diagnose BP elevation in early life includes measurement of BP any time a preterm-born child presents for health care.39 If our results can be confirmed, it would be appropriate to suggest routine follow-up of preterm-born infants with regard to BP. A more active approach to interventions in childhood may also be needed to avoid end-organ damage in adulthood.39
|
Acknowledgments |
|---|
This study was supported by a grant from Pfizer Sweden AB. Mikael Norman was supported by the Swedish Research Council (project No. 71P-14158).
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
- Sallout B, Walker M. The fetal origin of adult diseases. J Obstet Gynaecol. 2003; 23: 555–560.[CrossRef][Medline]
[Order article via Infotrieve]
- Leon DA, Lithell HO, Vagero D, Koupilova I, Mohsen R, Berglund L, Lithell UB, McKeigue PM. Reduced fetal growth rate and increased risk of death from ischaemic heart disease: cohort study of 15 000 Swedish men and women born 1915–29. BMJ. 1998; 317: 241–245.
[Abstract/Free Full Text]
- Martin JA, Hamilton BE, Sutton PD, Ventura SJ, Menacker F, Munson ML. Births: final data for 2002. Natl Vital Stat Rep. 2003; 52: 1–113.[Medline]
[Order article via Infotrieve]
- Huxley R, Neil A, Collins R. Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure? Lancet. 2002; 360: 659–665.[CrossRef][Medline]
[Order article via Infotrieve]
- Irving RJ, Belton NR, Elton RA, Walker BR. Adult cardiovascular risk factors in premature babies. Lancet. 2000; 355: 2135–2136.[CrossRef][Medline]
[Order article via Infotrieve]
- Doyle LW, Faber B, Callanan C, Morley R. Blood pressure in late adolescence and very low birth weight. Pediatrics. 2003; 111: 252–257.
[Abstract/Free Full Text]
- Jarvelin MR, Sovio U, King V, Lauren L, Xu B, McCarthy MI, Hartikainen AL, Laitinen J, Zitting P, Rantakallio P, Elliott P. Early life factors and blood pressure at age 31 years in the 1966 northern Finland birth cohort. Hypertension. 2004; 44: 838–846.
[Abstract/Free Full Text]
- Law CM, Shiell AW, Newsome CA, Syddall HE, Shinebourne EA, Fayers PM, Martyn CN, de Swiet MF. Fetal, infant, and childhood growth and adult blood pressure: a longitudinal study from birth to 22 years of age. Circulation. 2002; 105: 1088–1092.
[Abstract/Free Full Text]
- Kistner A, Jacobson L, Jacobson SH, Svensson E, Hellstrom A. Low gestational age associated with abnormal retinal vascularization and increased blood pressure in adult women. Pediatr Res. 2002; 51: 675–680.[CrossRef][Medline]
[Order article via Infotrieve]
- Edstedt-Bonamy A, Bendito A, Martin H, Andolf E, Sedin G, Norman M. Preterm birth contributes to increased vascular resistance and high blood pressure in adolescent girls. Pediatr Res. 2005; 85: 845–849.
- Kistner A, Celsi G, Vanpee M, Jacobson SH. Increased blood pressure but normal renal function in adult women born preterm. Pediatr Nephrol. 2000; 15: 215–220.[CrossRef][Medline]
[Order article via Infotrieve]
- Lundgren EM, Cnattingius HM, Jonsson GB, Tuvemo TH. Linear catch-up growth does not increase the risk of elevated blood pressure and reduces the risk of overweight in males. J Hypertens. 2001; 19: 1533–1538.[CrossRef][Medline]
[Order article via Infotrieve]
- Leon DA, Johansson M, Rasmussen F. Gestational age and growth rate of fetal mass are inversely associated with systolic blood pressure in young adults: an epidemiologic study of 165,136 Swedish men aged 18 years. Am J Epidemiol. 2000; 152: 597–604.
[Abstract/Free Full Text]
- Siewert-Delle A, Ljungman S. The impact of birth weight and gestational age on blood pressure in adult life: a population-based study of 49-year-old men. Am J Hypertens. 1998; 11 (pt 1): 946–953.[CrossRef][Medline]
[Order article via Infotrieve]
- Clausson B, Lichtenstein P, Cnattingius S. Genetic influence on birthweight and gestational length determined by studies in offspring of twins. Br J Obstet Gynaecol. 2000; 107: 375–381.
- Cnattingius S, Granath F, Petersson G, Harlow BL. The influence of gestational age and smoking habits on the risk of subsequent preterm deliveries. N Engl J Med. 1999; 341: 943–948.
[Abstract/Free Full Text]
- Marenberg ME, Risch N, Berkman LF, Floderus B, de Faire U. Genetic susceptibility to death from coronary heart disease in a study of twins. N Engl J Med. 1994; 330: 1041–1046.
[Abstract/Free Full Text]
- Wannamethee SG, Whincup PH, Shaper G, Walker M. Influence of fathers’ social class on cardiovascular disease in middle-aged men. Lancet. 1996; 348: 1259–1263.[CrossRef][Medline]
[Order article via Infotrieve]
- Marsal K, Persson PH, Larsen T, Lilja H, Selbing A, Sultan B. Intrauterine growth curves based on ultrasonically estimated foetal weights. Acta Paediatr. 1996; 85: 843–848.[Medline]
[Order article via Infotrieve]
- The Swedish Medical Birth Register: a summary of content and quality. Stockholm, Sweden: National Board of Health and Welfare; 2003. Available at: http://www.sos.se/fulltext/112/2003-112-3/2003-112–3.pdf. Accessed November 11, 2005.
- Population and Housing Census 1990, Part 7: the Planning and Processing of the Population and Housing Census. Stockholm: Statistics Sweden; 1992.
- Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United States national reference for fetal growth. Obstet Gynecol. 1996; 87: 163–168.[Abstract]
- Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003; 42: 1206–1252.
[Abstract/Free Full Text]
- Obesity: preventing and managing the global epidemic. Report of a WHO consultation. WHO Tech Rep Ser. 2000; 894: 1–253.
- Gournay V, Drouin E, Roze JC. Development of baroreflex control of heart rate in preterm and full term infants. Arch Dis Child Fetal Neonatal Ed. 2002; 86: F151–F154.
[Abstract/Free Full Text]
- Mitanchez-Mokhtari D, Lahlou N, Kieffer F, Magny JF, Roger M, Voyer M. Both relative insulin resistance and defective islet beta-cell processing of proinsulin are responsible for transient hyperglycemia in extremely preterm infants. Pediatrics. 2004; 113 (pt 1): 537–541.
[Abstract/Free Full Text]
- Plagemann A, Harder T, Rake A, Voits M, Fink H, Rohde W, Dorner G. Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats. Brain Res. 1999; 836: 146–155.[CrossRef][Medline]
[Order article via Infotrieve]
- Levitt NS, Lambert EV, Woods D, Hales CN, Andrew R, Seckl JR. Impaired glucose tolerance and elevated blood pressure in low birth weight, nonobese, young south African adults: early programming of cortisol axis. J Clin Endocrinol Metab. 2000; 85: 4611–4618.
[Abstract/Free Full Text]
- Ng PC, Lee CH, Lam CW, Ma KC, Fok TF, Chan IH, Wong E. Transient adrenocortical insufficiency of prematurity and systemic hypotension in very low birthweight infants. Arch Dis Child Fetal Neonatal Ed. 2004; 89: F119–F126.
[Abstract/Free Full Text]
- Weaver IC, Cervoni N, Champagne FA, D’Alessio AC, Sharma S, Seckl JR, Dymov S, Szyf M, Meaney MJ. Epigenetic programming by maternal behavior. Nat Neurosci. 2004; 7: 847–854.[CrossRef][Medline]
[Order article via Infotrieve]
- Singhal A, Cole TJ, Lucas A. Early nutrition in preterm infants and later blood pressure: two cohorts after randomised trials. Lancet. 2001; 357: 413–419.[CrossRef][Medline]
[Order article via Infotrieve]
- Singhal A, Fewtrell M, Cole TJ, Lucas A. Low nutrient intake and early growth for later insulin resistance in adolescents born preterm. Lancet. 2003; 361: 1089–1097.[CrossRef][Medline]
[Order article via Infotrieve]
- Norman M, Martin H. Preterm birth attenuates association between low birth weight and endothelial dysfunction. Circulation. 2003; 108: 996–1001.
[Abstract/Free Full Text]
- Singhal A, Cole TJ, Fewtrell M, Deanfield J, Lucas A. Is slower early growth beneficial for long-term cardiovascular health? Circulation. 2004; 109: 1108–1113.
[Abstract/Free Full Text]
- Taipale P, Hiilesmaa V. Predicting delivery date by ultrasound and last menstrual period in early gestation. Obstet Gynecol. 2001; 97: 189–194.
[Abstract/Free Full Text]
- Kramer MS, Platt R, Yang H, Joseph KS, Wen SW, Morin L, Usher RH. Secular trends in preterm birth: a hospital-based cohort study. JAMA. 1998; 280: 1849–1854.
[Abstract/Free Full Text]
- Morley R, Leeson Payne C, Lister G, Lucas A. Maternal smoking and blood pressure in 7.5 to 8 year old offspring. Arch Dis Child. 1995; 72: 120–124.[Abstract]
- Vatten LJ, Romundstad PR, Holmen TL, Hsieh CC, Trichopoulos D, Stuver SO. Intrauterine exposure to preeclampsia and adolescent blood pressure, body size, and age at menarche in female offspring. Obstet Gynecol. 2003; 101: 529–533.
[Abstract/Free Full Text]
- The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004; 114 (suppl 4th report): 555–576.
[Free Full Text]
This article has been cited by other articles:
 |
|
 |
|
  L. L. Hui, C. M. Schooling, S. S. L. Leung, K. H. Mak, L. M. Ho, T. H. Lam, and G. M. Leung Birth Weight, Infant Growth, and Childhood Body Mass Index: Hong Kong's Children of 1997 Birth Cohort Arch Pediatr Adolesc Med, March 1, 2008; 162(3): 212 - 218. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. H. Willemsen, S. W. K. de Kort, D. C. M. van der Kaay, and A. C. S. Hokken-Koelega Independent Effects of Prematurity on Metabolic and Cardiovascular Risk Factors in Short Small-for-Gestational-Age Children J. Clin. Endocrinol. Metab., February 1, 2008; 93(2): 452 - 458. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Palinski and C. Napoli Impaired Fetal Growth, Cardiovascular Disease, and the Need to Move on Circulation, January 22, 2008; 117(3): 341 - 343. [Full Text] [PDF]
|
|
|
|
|
|
M. Kaijser, A.-K. E. Bonamy, O. Akre, S. Cnattingius, F. Granath, M. Norman, and A. Ekbom Perinatal Risk Factors for Ischemic Heart Disease: Disentangling the Roles of Birth Weight and Preterm Birth Circulation, January 22, 2008; 117(3): 405 - 410. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Boubred, C. Buffat, J.-M. Feuerstein, L. Daniel, M. Tsimaratos, C. Oliver, M. Lelievre-Pegorier, and U. Simeoni Effects of early postnatal hypernutrition on nephron number and long-term renal function and structure in rats Am J Physiol Renal Physiol, December 1, 2007; 293(6): F1944 - F1949. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. R Dalziel, V. Parag, A. Rodgers, and J. E Harding Cardiovascular risk factors at age 30 following pre-term birth Int. J. Epidemiol., August 1, 2007; 36(4): 907 - 915. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A. Lawlor, A. Hubinette, P. Tynelius, D. A. Leon, G. D. Smith, and F. Rasmussen Associations of Gestational Age and Intrauterine Growth With Systolic Blood Pressure in a Family-Based Study of 386 485 Men in 331 089 Families Circulation, February 6, 2007; 115(5): 562 - 568. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||