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Relation between birth weight at term and systolic blood pressure in adolescence

University of WAles College of Medicine, Heath Park, Cardiff C4 4XN Correspondence to: Professor Davies.

Abstract

Objective : To examine whether birth weight is related to systolic blood pressure during adolescence.
Design : Retrospective (comparative) cohort study. The observers who traced and studied the subjects were unaware of their case-control status.
Subjects : 330 subjects were born in Cardiff in 1975-7. Cases who were low birth weight at term (<2500 g) were matched with controls of normal birth weight (3000-3800 g) at term.
Main outcome measures : Systolic blood pressure measured by random zero sphygmomanometry in the subject's right arm with the subject supine, corrected for size and age.
Results : The mean age at examination was 15.7 years. The mean systolic blood pressure of the cases was 105.8mm Hg and of the controls 107.5 mm Hg. The corrected difference (95% confidence interval) in systolic blood pressure between the cases and controls was 1 mm Hg (-3 to +1 mm Hg; two tailed probability 0.33).
Conclusion : Systolic blood pressure in adolescents of low birth weight is not significantly different from that of adolescents of normal birth weights.

Introduction

Hypertension is a well accepted risk factor for ischaemic heart disease and stroke. To the known risk factors for hypertension of obesity,^1,2 lifestyle,^3,4 and increased salt intake⁵ has recently been added low growth rate in utero with its proxy of low birth weight at term.*RF 6-9* The hypothesis advanced is that programming of physiological or metabolic events caused by undernutrition¹⁰ at critical or sensitive periods early in life can amplify certain long term changes which eventually manifest in disease, in this case hypertension and ischaemic heart disease. Evidence for this hypothesis comes largely from studies of cohorts born in Britain earlier this century, most of whom were men.*RF 6-9* A criticism of these studies is that people whose growth has been affected in early development may continue to have imposed during childhood and adult life a hostile environment that leads eventually to disease.¹¹ The confounding influence of these external environmental effects may be evident in advance of the consequences of the intrauterine environment. Also in some circumstances the extrauterine effects may be overwhelming.

We aimed to minimise the effects of different extrauterine environments by investigating the association between low birth weight at term with systolic blood pressure in schoolchildren.

Subjects and methods Study design

This was a retrospective cohort study in which the subjects were traced and assessed by observers who were unaware of whether they were cases or controls. A strict protocol was drawn up for the identification and selection of subjects, methods of clinical examination, and statistical analysis. Ethical approval was granted by the South Glamorgan Health Authority and the local family health services authority.

Tracking of systolic blood pressure is well documented throughout childhood and adult life.¹² Raised blood pressure may be amplified throughout life so that any differences associated with low birth weight may become larger with advancing age.¹³ If very young children were studied tracing might be easier as few would have changed address, but any differences in blood pressure due to prenatal experiences might be small. Older children would be more difficult to find, but the differences in blood pressure might be larger. Children in school are a fairly easy group to locate with the availability of computerised school health records, and they are a homogeneous group whose environment is similar for part of the day so that some confounding variables (which might begin to impose themselves when the subject leaves school - for example, occupation) would be lessened.

Cases and controls were identified from the Cardiff birth survey. Every birth in Cardiff and later in South Glamorgan has been documented since 1965. Cases were defined as infants with a birth weight under 2500 g at 38 weeks' gestation or more, a group likely to have suffered retardation of intrauterine growth. Unlike low birth weight and preterm delivery there is no internationally agreed definition of fetal growth retardation. Controls were infants born at 38 weeks' gestation or more and weighing 3000-3800 g. These infants were judged to have grown adequately in utero.

Multiple pregnancies and infants with congenital abnormalities were excluded, as were deaths and medical conditions that might influence systolic blood pressure. Only births at the two large obstetric departments were used as the small numbers born elsewhere would not have sufficient well matched controls. There were 8920 relevant deliveries during the study.

The initial variables used to calculate sample size were (alpha)=0.05 and ß=0.10, and the smallest difference in systolic blood pressure that could be viewed as clinically important was 4mm Hg. No estimate of the standard deviation of the differences in systolic blood pressure between cases and controls matched as described was available. The estimated standard deviation of systolic blood pressure for 15 year olds was 12 mm Hg,¹⁴ giving a standardised difference of 4/12=0.33. Without matched data a sample size of between 173 and 234 in each group at analysis would be required. The data from the birth survey showed that the academic year cohorts from 1 September 1975 to 30 August 1977 would yield 230 potential cases. At the start of the study (March 1991) all were expected to be receiving compulsory full time education. If the matching were to reduce the variance then a greater power would ensue.¹⁵

Matching of cases and controls

For each index case a list of eligible controls was drawn up with a computer. Cases and controls were matched for sex, hospital of delivery, parity of the mother, date of birth, and length of gestation. Length of gestation was calculated from the mother's last menstrual period as ultrasound scanning was not routinely available. If there was doubt regarding length of gestation a Dubowitz assessment of the neonate was performed. Prior rules for selection of controls were applied in sequence until a match was found. These rules were designed so that if any bias was introduced by matching it would result in the cases having a higher systolic blood pressure than the controls, which is in favour of the alternative hypothesis.

Data collected

Data on the mother collected at delivery included social, lifestyle, and clinical variables associated with the current pregnancy and relevant medical history. Data on the infant included details of the delivery and relevant clinical variables. The following multiple sources were used to trace the subjects: computerised school records, South Glamogran family health services authority, NHS central register (including armed forces), telephone directory, South Glamorgan Social Services, hospital patient administration system, general practitioners, door to door inquiries, hospital records at the time of delivery (which occasionally contained telephone numbers of relatives), and the medical directory.

The subjects who agreed to participate were visited at home by one of two observers who had been trained in the techniques of anthropometry and measurement of blood pressure.

Weight was measured to the nearest 100 g with the subject lightly clothed and without shoes by using a portable Soehnle scale. Height was measured by using a portable Harpenden stadiometer to the nearest 1 mm. Systolic blood pressure was measured with a random zero sphygmomanometer by following recommendations of the British Hypertension Society.¹⁶

Analysis

The statistical package SPSS/PC was used for analysis.¹⁷ Means were compared by using a paired t test. The effect on systolic blood pressure of sex was examined by using one way analysis of variance, and the effect of birth weight, maternal height, and gestation was determined by using the non-parametric Kruskal-Wallis test. Results were all rounded after calculation.

Results

Of 230 potential low birthweight cases identified, eight were ineligible (six were dead and two had medical conditions not recorded at birth (pseudohypoparathyroidism and severe cerebral palsy)), leaving a cohort of 222. The records of five were marked as "confidential - not to be used for research studies"; four subjects were living too far from Cardiff to visit, 17 subjects could not be traced at all, and 19 refused to participate. A total of 177 cases were finally studied.

Of the controls for these cases, 75% (133/177) were found. When it was recognised early in the study that a control would be unavailable a subsequent control was drawn. For the 30 identified subsequent controls, 93% (28) were seen. This left 12 cases who were seen but did not have matched controls and could not therefore be used in the paired analysis. In total 74% (165/222) of the case-control pairs were found. The subjects studied were of mean age 15.7 years. In one control the weight had not been recorded.

We did not consider it appropriate to determine the exact stage of puberty during a home visit. Tables I and II show the closeness of the case-control matching. Table III gives a comparison of the cases and controls. There were important differences in age, height, and weight at examination which influence systolic blood pressure. These differences may be adjusted for by fitting a linear regression model to the data.¹⁸ No existing model was suitable so age, height, weight, sex, body mass index (weight (kg)/(height (m)²)), and case-control status were entered into a stepwise multiple regression to produce a linear model for systolic blood pressure. All the available data were used. The best fit to the data was: systolic blood pressure=24.7+0.31 weight (kg) + 4.1 age (years); r²=0.24; SE weight coefficient=0.05; SE age coefficient=0.69.

TABLE I - Summary of differences in parity of mothers of cases and controls
for each pair of subjects
-----------------------------------------
Parity      Difference in parity (cases
for             minus controls)
mothers     -----------------------------
of cases      -2    -1     0     +1
-----------------------------------------
0                          82
1                    1     49     1
2                          18     1
3              1            6     2
4                    1      2
5                           1
-----------------------------------------
Total          1     2    158     4

TABLE II - Summary of differences in length of gestation between cases and
controls for each pair of subjects
----------------------------------------
Length      Differences in length of
of         gestation (weeks) for cases
gestation       minus controls
(weeks)    ----------------------------
for cases      -1       0       +1
---------------------------------------
38              2      41        4
39                     40
40                     62
41                     13
42              1       2
--------------------------------------
Total           3     158        4

TABLE III - Comparison between 165 cases and 165 controls. Data on birth
weight and maternal height from Cardiff birth survey, other data from
examination of adolescents
-------------------------------------------------------------------------------------------
                                         Mean      SD      Median      Minimum      Maximum
-------------------------------------------------------------------------------------------
Birth weight (coded to nearest 100 g):
Cases                                   2250               2300         1600         2400
Controls                                3330               3300         3000         3800
Maternal height (inches)*:
Cases                                     61.9               68.0         57.0         67.0
Controls                                  62.7               63.0         57.0         67.0
Body mass index (kg/m2:
Cases                                     20.2     3.1       19.9         12.9         29.0
Controls                                  21.1     3.7       20.7         13.4         35.8
Difference                                -0.93    4.9       -0.4         10.6        -18.1
Age at examination (years):
Cases                                     15.6     0.77      15.45        14.1         17.3
Controls                                  15.8     0.84      15.7         14.0         17.8
Difference (days)                        -74.6   286        -53          550         -722
Systolic blood pressure
Cases                                    105.8    10.2      105           82          136
Controls                                 109.5    11.5      108           78          144
Difference                                -3.8    14.4       -2           32          -48
Weight (kg):
Cases                                     52.1     9.0       51.4         33.4         80.0
Controls                                  58.4    11.7       57.1         33.0        110.6
Difference                                -6.3    14.7       -5.5         28.8        -71.8
Height (cm):
Cases                                    160.7     7.72     160.9        134.0        185.0
Controls                                 166.1     7.96     165.1        148.0        185.1
Difference                                -5.4     9.6       -5.0         20.2       -233.3
-------------------------------------------------------------------------------------------
 *Data recorded for 161 cases and 161 controls to nearest inch with extreme
values coded as <=57" (145 cm) and >=67" (170 cm).

This model was then used to adjust the paired differences in systolic blood pressure. For one subject the weight was not available and so adjusted systolic blood pressure could not be calculated. The mean (SD) difference in adjusted systolic blood pressure for the 164 remaining pairs of subjects was -1.0 (13.0)mm Hg, with a median of 0.35, minimum of - 41.4, and maximum of 33.2. The standard error was 1.01 and 95% confidence interval -3.0 to 1.0, giving a two tailed P value of 0.33. Table IV gives the non-significant differences in systolic blood pressure by sex. The effect of birth weight of cases (P=0.85), maternal height for cases (P=0.60), and length of gestation (P=0.66) on systolic blood pressure were all found to be non-significant by using the Kruskal-Wallis test, there being no obvious trend in the results.

Table IV Difference in adjusted systolic blood pressure by sex*
------------------------------------------------------------------------------
Sex             No of                                        95% Confidence
                subjects     Mean (SD)       SE              interval
------------------------------------------------------------------------------
Male              63       -1.4 (11.9)       1.5              -4.4 to 1.6
Female            101      -0.7 (13.6)       1.4              -3.4 to 2.0
------------------------------------------------------------------------------
 *(???) Ratio = 0.11, df = 1, P = 0.73. Tests equality of variance in two
groups gives P = 0.25.

Discussion

Infants who weighed less than 2500 g at 38 weeks' gestation or more (cases) are considered to have probably suffered retardation of growth in utero. These infants have a lower than average ponderal index because of fetal undernutrition from various causes.¹⁹ The control infants, on the other hand, were considered to have been adequately nourished during gestation.

This is the first reported population based comparative study to investigate the influence of low birth weight at term on later blood pressure. No link could be found between birth weight and blood pressure in adolescence once the differences in size and age between the two groups at examination were considered. Other studies have also failed to find an association. In a previous study mean systolic blood pressure of very low birthweight preterm children aged 8 years was 1.8 mm Hg lower than that of normal birth weight controls, but no correction was made for body size.²⁰ Cook et al found no association between birth weight and blood pressure in first degree relatives (mean age 43 years) of people with non-insulin dependent diabetes mellitus.²¹ A study from New Zealand showed that corrected systolic blood pressure in 7 year olds was 1 mm Hg higher in those who had suffered retardation of intrauterine growth compared with those of birth weight between the 10th and 90th centiles, but at the age of 18 years the differences were not significant.²² In nearly 33 000 men and women aged 17 years Seidman et al found that systolic blood pressure was positively associated with birth weight, but the correlation coefficients were low; current body weight was significantly associated with systolic blood pressure, suggesting that an adverse extrauterine environment was a much more important determinant of blood pressure than birth weight.¹⁸

Other studies have found associations between birth weight and later blood pressure. Multiple regression analysis of factors affecting systolic blood pressure in Croatian subjects aged 18-23 years showed an inverse relation with birth weight.²³ In 36 year old subjects from the Medical Research Council's 1946 birth cohort systolic blood pressure fell by 2.6 mm Hg in men and 1.8 mm Hg in women from the highest to the lowest third of the distribution of birth weight.⁷ A study of men and women aged 50 years from Preston found that a higher systolic blood pressure was related to increased placental weight and lower birth weight.⁶ Barker et al found a similar relation between low birth weight and increasing systolic blood pressure in men aged 59-70 years in Hertfordshire.⁸ Higher standardised mortality ratios for ischaemic heart disease in men in Sheffield were associated with low birth weight, small head circumferences, and reduced ponderal indices at birth.⁹ Whincup et al studied children aged 5-7 years and found a relation between low birth weight and systolic blood pressure corrected for age, sex, height, and body mass index.²⁴ The effect was similar for prematurity and growth retardation, and one suggested explanation was that increased postnatal growth rates might be more important in determining future blood pressure than prenatal growth.

Sources of bias

Many of these studies rely on cohorts born a long time ago, when health care practices, environmental conditions, and diet were probably different.*RF 6,8-10* Also only the survivors from times when infant mortality was high have been studied. These factors could be a source of bias. Different factors may now predispose to intrauterine growth retardation - for example, maternal smoking. Several groups have questioned whether the links between intrauterine growth retardation and later disease might be explained by a continuum of social and environmental insults throughout life.*RF 25-28* Our findings of no link at the age of 15 years may be because any possible adverse life style has not yet had sufficient time to exert an effect.

The possibility of a "false negative" result can never be discounted. There are two sources of bias which may have influenced our study: case ascertainment bias and recruitment bias. Case ascertainment bias may lead to important subgroups being underrepresented in the sample. Here we failed to use 57 cases (25%). Control selection and ascertainment bias may similarly lead to underrepresentation of important subgroups. Attempts were made to control these types of potential bias by keeping the field workers blind to subjects' case-control status. Also the controls were selected by using prior rules which entailed no additional judgment. The strength of the study lies in the fact that it is based on the population of a well defined geographical location, every member of that population being recorded. While the number of cases (165) may seem small compared with other studies with much larger samples the effective population studied here is over 9000 with just the cases of particular interest selected.

Conclusion

s

Our results are inconsistent with adolescents born at term with low birth weight having a systolic blood pressure more than 1 mm Hg above or more than 3 mm Hg below that of controls with normal birth weight. This result lends no support to the hypothesis that low birth weight at term is related to a higher blood pressure during adolescence.

The hypothesis that hypertension may be initiated in fetal life is fascinating and derives additional support from studies on animals. Before it shifts from hypothesis to established fact, however, further large population studies are required to determine any association between birth weight (a proxy for changes in structure, physiology, and metabolism determined in utero) and blood pressure through the whole span of life.

This study was supported by a grant from Children Nationwide. We thank the steering committee of the Cardiff birth survey for the use of the data, and Mrs D Savory, who conducted much of the fieldwork. We are also greatful for the willing cooperation of all of the subjects.

1. Higgins M, Kannel W, Garrison R, Pinsky J, Stokes J. Hazards of obesity - the Framingham experience. Acta Med Scand 1988;suppl 723:23-36.
2. Aristimuno GG, Foster TA, Voors AW, Srinivasan Sr, Berenson GS. Influence of persistent obesity in children on cardiovascular risk factors - the Bogolusa heart study. Circulation 1984;69:895-904. [Abstract/Free Full Text]
3. Poulter NR, Thaw KT, Hopwood BEC, Mugambi M, Peart WS, Rose G, et al. The Kenyan Luo migration study: observations on the initiation of a rise in blood pressure. BMJ 1990;300:967-72.
4. Timio M, Verdecchia P, Venanzi S, Gentili S, Ronconi M, Francucci B, et al. Age and blood pressure changes. A 20 year follow up study in nuns in a secluded order. Hypertension 1988;12:457-61. [Abstract/Free Full Text]
5. Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction lower blood pressure? BMJ 1991;302:811-24.
6. Barker DJP, Bull AR, Osmond C, Simmonds SJ. Fetal and placental size and risk of hypertension in adult life. BMJ 1990;301:259-62.
7. Barker DJP, Osmond C, Golding J, Kuh D, Wadsworth MEJ. Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. BMJ 1989;298:564-7.
8. Barker DJP, Meade TW, Fall CHD, Lee A, Osmond C, Phipps K, et al. Relation of fetal and infant growth to plasma fibrinogen, and factor VII concentrations in adult life. BMJ 1992;304:148-52.
9. Barker DJP, Osmond C, Simmonds SJ, Wield GA. The relation of head size and thinness at birth to death from cardiovascular disease in adult life. BMJ 1993;306:422-6.
10. Barker DJP, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS. Fetal nutrition and cardiovascular disease in adult life. Lancet 1993;341:938-41. [Medline]
11. Eames M, Ben-Shlomo Y, Marmot MG. Social deprivation and premature mortality: regional comparison across England. BMJ 1993;307:1097-102.
12. Gillman MW, Cook NR, Rosner B, Keough ME, Taylor JO, Hennekens CH. Identifying children at high risk for the development of essential hypertension. J Pediatr 1993;122:837-46. [Medline]
13. Law CM, de Swiet M, Osmond C, Fayers PM, Barker DJP, Cruddas AM, et al. Initiation of hypertension in utero and its amplification throughout life. BMJ 1993;306:24-7.
14. Task force on blood pressure control in children. National heart, lung and blood institute, Bethesda, Maryland. Report of the Second Task Force on Blood Pressure Control in Children - 1987. Pediatrics 1987;79:1-25. [Abstract/Free Full Text]
15. Machin D, Campbell MJ. Statistical tables for the design of clinical trials. Oxford: Blackwell Scientific, 1987.
16. Petrie JC, O'Brien ET, Little WA, de Swiet M. Recommendations on blood pressure measurement. BMJ 1986;293:611-5.
17. Norusis MJ. Statistical package for the social sciences. SPSS/PC+4.0 base manual. Chicago: SPSS, 1990.
18. Seidman DS, Laor A, Gale R, Stevenson DK, Mashiach S, Danon YL. Birth weight, current body weight and blood pressure in late adolescence. BMJ 1991;302:1235-7.
19. Davies DP, Platts P, Pritchard JM, Wilkinson PW. Nutritional status of light-for-dates infants at birth and its influence on early postnatal growth. Arch Dis Child 1979;54:703-6. [Abstract/Free Full Text]
20. Hack M, Weissman B, Breslau N, Klein N, Borawski Clark E, et al. Health of very low birth weight children during their first eight years. J Pediatr 1993;122:887-92. [Medline]
21. JTE Cook, Levy JC, Page RCL, Shaw JAG, Hattersley AT, Turner RC. Association of low birth weight with (beta) cell dysfunction in the first degree relatives of non-insulin dependent diabetic subjects. BMJ 1993;306:302-6.
22. Williams S, St George IM, Silva PA. Intrauterine growth retardation and blood pressure at age seven and eighteen. J Clin Epidemiol 1992;45:1257-63. [Medline]
23. Kolacek S, Kapetanovic T, Luzar V. Early determinants of cardiovascular risk factors in adults. B. Blood pressure. Acta Paediatr 1993;82:377-82. [Medline]
24. Whincup PH, Cook DG, Papacosta O. Do maternal and intrauterine factors influence blood pressure in childhood? Arch Dis Child 1992;67:1423-9.
25. Elford J, Shaper AG, Whincup P. Early life experiences and cardiovascular disease - ecological studies. J Epidemiol Community Health. 1992;46:1-11.
26. Elford J, Whincup P, Shaper AG. Early life experiences and adult cardiovascular disease: Longitudinal and case-control studies. Int J Epidemiol 1991;20:833-44. [Abstract/Free Full Text]
27. Ben-Shlomo, Davey Smith G. Deprivation in infancy or adult life; which is more important for mortality risk? Lancet 1991;337:530-4.
28. Davies DP, Matthes JWA. Fetal and infant growth and impaired glucose tolerance. BMJ 1991;303:1474.

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Birth weight and blood pressure in adolescence studies may be misleading

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