(Stroke. 2000;31:869.)
© 2000 American Heart Association, Inc.
Original Contributions |
Early Growth, Adult Income, and Risk of Stroke
From the National Public Health Institute, Department of Epidemiology and Health Promotion, Diabetes and Genetic Epidemiology Unit, Helsinki, Finland (J.G.E., T.F., J.T.), and the Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK (C.O., D.J.P.B.).
Correspondence to Prof D.J.P. Barker, Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK. E-mail david.barker{at}mrc.soton.ac.uk
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Abstract |
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Background and Purpose—A number of studies have shown that reduced intrauterine growth and low birth weight are associated with raised rates of fatal and nonfatal stroke in adult life. Whether this increased risk of stroke is modified by growth in childhood or by socioeconomic status in adult life is not known.
Methods—We studied hospital admissions and deaths from stroke among 3639 men who were born in Helsinki University Central Hospital during 1924 to 1933. They had detailed records of their body size at birth, their growth through childhood, and their social circumstances as adults. Three hundred thirty-one of the men had had a stroke.
Results—Hazard ratios for stroke were related to low birth weight in relation to head circumference (P=0.005) and to short length in relation to head circumference (P=0.02). These associations were stronger for hemorrhagic than for thrombotic stroke. Men who developed stroke still had below-average stature at 7 years (P=0.05), but after 7 years their height "caught up" through accelerated growth. As adults they had low incomes and low social class (P<0.0001).
Conclusions—Stroke may originate through reduced fetal growth, with low body weight and short body length at birth but "sparing" of head growth. Other studies suggest that this pattern of growth is associated with persisting elevation of blood pressure and raised plasma fibrinogen concentrations, 2 known risk factors for stroke. The risk of stroke is increased by accelerated growth in height during childhood. Accelerated growth has previously been linked to the development of hypertension in adult life. Stroke risk is further increased by adverse influences linked to low income.
Key Words: child • fetal growth retardation • growth • social class • stroke
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Introduction |
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Follow-up studies in the United Kingdom,1 Sweden,2 and the United States3 have shown that low birth weight is associated with an increased risk of fatal and nonfatal stroke in adult life. This has led to the hypothesis that stroke originates in utero. This is part of a more general hypothesis, the "fetal origins hypothesis," which proposes that cardiovascular disease and non–insulin-dependent diabetes originate through adaptations made by the fetus when it is undernourished.4 5 In one of the studies, in Sheffield, United Kingdom, measurements of body size at birth in addition to birth weight were available. Death from stroke was more strongly associated with low birth weight in relation to head circumference at birth than with low birth weight alone.1 A conclusion from this was that stroke may originate through "brain-sparing" adaptations in fetal growth.
We have recently described the associations between body size at birth and coronary heart disease in a cohort of men born in Helsinki during 1924 to 1933.6 Ninety-two percent of the men were still residents in Finland in 1971, and subsequent hospital admissions and deaths among them were ascertained through national registers. We describe here the associations between body size at birth and stroke. The database for the cohort also includes information on childhood growth and social class and income in adult life. We are therefore able to report for the first time how these influences, at different stages of life, modify the risk of stroke associated with poor growth in utero.
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Subjects and Methods |
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We studied a sample of 3639 men who were born at the Helsinki University Central Hospital. Details of the birth records have been described elsewhere.6 Data on the mothers consisted of age, parity, height, date of the last menstrual period, and body weight measured on admission in labor. The records also contained external measurements of the mother’s pelvis including the conjugate diameter (the distance between the symphysis pubis and the spine of the fifth lumbar vertebra), the intercristal diameter (the maximum width across the iliac crests), and the interspinous diameter (the distance between the anterior superior iliac spines). Data on the newborn babies consisted of birth weight, crown-to-heel length, head circumference, and placental weight. We studied men who were born at the hospital between 1924 and 1933, who went to school in Helsinki, and who still resided in Finland in 1971. School health records for all children attending school in Helsinki have been preserved, and details of the records have been described.7 They include an average of 10 (SD=4) measurements of height and weight between the ages of 6 and 16 years, recorded at periodic medical examinations. They also include the number of other people living in the child’s home, recorded at the time of the first examination, and the number of rooms. Since 1971 all residents of Finland have been assigned a unique personal identification number. From the birth and school records and identification numbers we identified 3815 men who were born in the Helsinki University Central Hospital, went to school in the city, and were living in Finland in 1971. One hundred seventy-six of these subsequently emigrated, and the date of emigration was not always recorded. We therefore excluded them from the study, leaving a total of 3639 (95%).
We used the personal identification number to identify all hospital admissions and deaths among the men during 1971 to 1995. All hospital admissions in Finland are recorded in the national hospital discharge register. All deaths are recorded in the national mortality register. The first 3 digits from the cause of admission or death were used to identify the occurrence of stroke. We subdivided stroke according to the following diagnostic categories given in the International Classification of Disease: hemorrhagic (ICD 430 to 431), thrombotic (ICD 432 to 436) and unclassified (ICD 437 to 438). Under this classification, "hemorrhagic" includes intracerebral and subarachnoid hemorrhage and "thrombotic" includes cerebral thrombosis, cerebral embolism, and other occlusion of the cerebral and precerebral arteries. Our diagnoses were based solely on the ICD, as we did not have the case records. Using the father’s occupation, which was on the birth records, we grouped the men according to a social classification used by the Central Statistical Office. Overall, 85% of the fathers were laborers. Through the Office of Statistics the personal identification numbers were used to identify data on adult social class and annual income obtained at the 1970/71 census.
Statistical Analysis
We examined the trends in hazard ratios for the first stroke
event with maternal, neonatal, and childhood measurements and with the
socioeconomic variables. Tests for trend were based on Cox’s
proportional hazards model. We converted each height, weight, and body
mass index measurement for each boy to a z score. We interpolated
between successive z scores with a piecewise linear function and so
obtained a z score at each birthday from age 7 to age 15. We back
transformed these z scores to obtain the corresponding height, weight,
and body mass index at these ages. We used the regression slope of the
z scores with age to measure the rate of growth in height, weight, and
body mass index from 7 to 15 years. We measured each child’s height
gain from age 7 to 15 years as the difference between the observed
values and those predicted from the heights at age 7 years.
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Results |
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The maternal, neonatal, and childhood characteristics of the men in the cohort have been published.7 Three hundred twelve of the 3639 men had been admitted to hospital for stroke; 58 of these had died from the disease. An additional 19 had died without hospital admission. We therefore analyzed 331 men with stroke. The annual death rate from stroke at age 45 to 64 years was 1.04 per 1000.
Size at Birth
Table 1
shows hazard
ratios for stroke, with hospital admissions and deaths combined and
deaths alone, according to size at birth. The ratios fell with
increasing birth weight up to 3500 g. Hazard ratios were not
related to head circumference, but Table 1 shows that the trends
with birth weight were strengthened by adjusting for head
circumference. The hazard ratio for admissions and deaths was 1.5 (95%
CI 1.1 to 2.1, P=0.005) for each kilogram decrease in birth
weight adjusted for head circumference. Hazard ratios also fell with
increasing length at birth (Table 1) and fell more strongly with
increasing length adjusted for head circumference. Addition of length
to a Cox model that included birth weight and head circumference did
not, however, improve the prediction of stroke. Hazard ratios fell with
increasing placental weight (P=0.03 for admissions and
deaths, P=0.5 for deaths). Placental weight was inversely
related to the ratio of head circumference to birth weight (correlation
coefficient -0.52). The hazard ratios were not related to the length
of gestation, and the trends shown in Table 1 were little
changed by adjustment for gestation.
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Growth in Childhood
The average height of men who developed stroke was 0.7 cm below
that of the other men at 7 years of age (P=0.05). Table 1
shows that hazard ratios fell across the range of height at 7
years. After 7 years of age, the difference in height between the men
who developed stroke and all other men progressively declined, which
indicates that stroke was related to an above-average rate of growth in
height between 7 and 15 years (P=0.05 for admissions and
deaths, P=0.03 for deaths). Changes in height between 7 and
15 years of age, in relation to the change predicted from the cohort as
a whole, are given in Table 1. Hazard ratios for stroke rose
with increasing height gain. In the cohort as a whole, boys who were
0.7 cm below average height at 7 years had heights that were 1.1 cm
below average by the age of 15 years. The high rate of height growth
from 7 to 15 years of age in boys who developed stroke was not,
therefore, a general pattern of catch-up growth associated with
stunting at age 7.
The average weight of men who developed stroke was 0.3 kg below that of the other men at 7 years of age (P=0.07). Similar to the trends with height, hazard ratios tended to fall across the range of weight at 7 years, though this was not statistically significant. In contrast to height, however, stroke was not related to an accelerated increase in weight after the age of 7 years. The mean body mass index from age 7 to 15 years of the men who died from stroke remained below that of all other men, though the difference was not statistically significant at any age.
Socioeconomic Status in Childhood
There were no statistically significant trends with social
class at birth in either admissions and deaths combined or in deaths
alone. The men grew up in houses that had on average 1.7 rooms (range 1
to 14). Forty-six percent of the houses had only 1 room. The number of
rooms in the house was not related to the subsequent development of
stroke. There were on average 4.5 other persons (range 1 to 27) in the
home during the men’s childhood. Hazard ratios for death from stroke
tended to rise with increasing numbers of people in the home
(P=0.02 for admissions and deaths, P=0.7 for
deaths). The number of people in the home was inversely related to the
children’s height at age 7 years (correlation coefficient -0.18), but
allowing for height in a simultaneous regression did not
change the association between number of people and stroke.
Socioeconomic Status in Adult Life
Table 1 shows that hazard ratios were higher among men who
had low social class as adults, and there was a sharp increase in
hazard ratios at adult incomes below 15 000 Finnish marks per year. In
a simultaneous regression with social class and income,
both trends in hazard ratios for admissions and deaths remained
statistically significant. The trends were little changed by adjusting
for birth weight, head circumference, and rate of height growth in
childhood.
Size at Birth and Socioeconomic Status
Table 1 shows that the trends in hazard ratios with size at
birth and height growth in childhood were little changed by adjusting
for social class and income in adult life. Table 2 shows the independent effects on stroke
of birth weight, adjusted for head circumference, and adult income. We
used 15 000 Finnish marks income per year to divide men with low and
high incomes. We assigned a hazard ratio of 1.0 to men in the highest
birth weight and income categories for admissions and deaths combined,
and separately for deaths alone. The highest hazard ratios, 2.3 for
admissions and deaths and 4.3 for deaths alone, were in the men who had
birth weights below 3000 g and low incomes.
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Maternal Characteristics
Hazard ratios for stroke tended to fall with increasing maternal
height though this trend was not statistically significant
(P=0.19 for admissions and deaths, P=0.13 for
deaths). They were not related to the mothers’ weights or body mass
indices during pregnancy or to maternal age and parity. The offspring
of shorter mothers had a higher ratio of head circumference to birth
weight than the offspring of taller mothers (correlation coefficient
-0.21). This effect of short maternal stature on body proportions at
birth was independent of the effect of placental weight on body
proportions.
Size at birth is known to be influenced by the size of the mother’s bony pelvis. The mean maternal external pelvic measurements were 19.4 cm for the external conjugate diameter, 28.4 cm for the intercristal diameter, and 25.9 cm for the interspinous diameter. One hundred fifty-three of the mothers had a flat pelvis, according to criteria used in clinical practice at the time8 : an external conjugate diameter of <7 inches (17.8 cm) and a difference between the intercristal and interspinous diameters of <1 inch (2.5 cm). Eighty-eight percent of the mothers with a flat pelvis were of below-average height (1.58 m). Flat pelvis was associated with an increased ratio of head circumference to birth weight (P<0.0001).
Hemorrhagic and Thrombotic Stroke
Sixty-two of the men had a hemorrhagic stroke, 247 had a
thrombotic stroke, and for 22 the type of stroke was not classified.
Table 3 shows that while both types of
stroke had similar trends with birth weight, the trend with birth
weight adjusted for head circumference was stronger for hemorrhagic
stroke. The trend in length adjusted for head circumference (Table 1) was apparent for hemorrhagic stroke (P=0.002) but
weaker for thrombotic stroke (P=0.14). The trends with
placental weight, childhood height growth, and adult social class and
income were similar for both types of stroke.
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Discussion |
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This study of men born in Helsinki, Finland, confirms previous observations that the risk of fatal and nonfatal stroke is associated with low birth weight, as a result of reduced rates of fetal growth.1 2 3 It also confirms the observation among men born in Sheffield, United Kingdom, that there is a stronger association with low birth weight in relation to head circumference.1 It shows for the first time that men who developed stroke had short body length at birth (especially in relation to their head circumference), were short at age 7 years, and had accelerated or "catch-up" growth in height thereafter. It also shows that the trends in stroke with low birth weight in relation to head circumference are independent of the increased risk of stroke associated with low social class and low income in adult life.
Our study was restricted to men who were born in Helsinki University Central Hospital. This would introduce a bias only if the association between size at birth and stroke differed between those born in this hospital and those born elsewhere. The fathers of 84% of the men were classified as laborers. The men may, therefore, not be representative of all men living in Helsinki, although we know that in the early years of this century approximately 60% of men in the city were laborers. We ascertained the occurrence of stroke through the national mortality and national hospital discharge registers. The validity of these registers has been previously reported.9 10 11 12 The diagnosis of stroke in the International Classification of Diseases, which we used, includes both hemorrhagic and thrombotic stroke. In general, we found stronger associations with fatal stroke than with nonfatal and fatal stroke combined.
Our finding that stroke is associated with low birth weight in relation to head circumference, and with short body length in relation to head circumference, supports the hypothesis that the disease originates through patterns of reduced fetal growth in which the brain is spared.1 We found that "brain sparing" was more closely associated with hemorrhagic than with thrombotic stroke. One brain-sparing mechanism is redistribution of cardiac output to favor the brain at the expense of the trunk.13 The structure of fetal arteries adapts to the blood flow and pressure within them,14 and redistribution of cardiac output may therefore permanently change the structure of the major arteries. One aspect of this change is reduced deposition of elastin, which is mostly laid down in utero and thereafter turns over slowly.15 There is indirect evidence that reduced blood flow in the major arteries of the trunk during fetal life may lead to persistently reduced elasticity and consequent raised blood pressure, a major risk factor for hemorrhagic stroke.16 Another consequence of redistribution of cardiac output is that development of the abdominal organs, including the liver, is compromised, and preliminary evidence suggests that this may lead to lifelong changes in liver function, with raised plasma fibrinogen concentrations,17 a known risk factor for thrombotic stroke.18 A third possible link between reduced fetal growth and stroke is that low birth weight has been shown to be strongly associated with an increased risk of carotid artery stenosis, suggesting that it is linked to increased atherogenesis.19
The fetal origins hypothesis proposes that cardiovascular disease originates through fetal undernutrition. Consistent with the findings in the Sheffield cohort we found that stroke was associated with low placental weight.1 Inadequate placental growth could lead to fetal undernutrition, inability to sustain fetal growth in late gestation, and consequent low birth weight in relation to head circumference. We have found that short maternal stature is another influence that leads to low birth weight in relation to head circumference. We have also confirmed that flat pelvis is linked to this pattern of fetal growth.1 Flat pelvis is more common in women who have short stature and poor general physique, and it originates through malnutrition in childhood.20 21 Our findings support the hypothesis that stroke may originate through chronic malnutrition of girls and young women and consequent inability to sustain the growth of their fetuses.1
We have been able to examine the childhood growth of men who developed stroke. They were short at birth and remained short, with below average weight, until they were 7 years of age. This is consistent with the observation that men in Hertfordshire, United Kingdom, who had low weight during infancy as well as at birth were at increased risk of stroke.1 Our findings suggest that large numbers of people in the home, with consequent high rates of enteric and respiratory infection, could be one explanation for this failure to catch up in height until later in childhood.22 After 7 years of age, the men had high rates of growth in height through childhood though remaining thin. It has been suggested that rapid growth in childhood leads to the development of essential hypertension, a risk factor for stroke.23 Children and adolescents who are growing more rapidly have high blood pressure for their age. Because blood pressure "tracks" through childhood, this leads to higher blood pressure in early adult life, a more rapid increase in blood pressure with age, and a greater risk of hypertension in later life. These observations have led to the hypothesis that essential hypertension is determined by 2 separate mechanisms, a growth-promoting process in childhood and a self-perpetuating mechanism in adult life.23
Stroke was not related to the father’s occupation at the time of
birth. It was, however, strongly related to low occupational status and
low income in adult life. Stroke is known to be more common among
less-affluent people.24 Though the reasons for this are
largely unknown, one possibility is that in northern European countries
poorer people tend to have lower intakes of fruit and green
vegetables.25 Low plasma vitamin C concentrations have
been shown to increase the risk of stroke.26 27 28 Whatever
the nature of the adverse influences associated with low income, our
analysis shows that its effects add to those of low birth
weight in relation to head circumference (Table 2).
We conclude that men who suffered a fatal or nonfatal stroke sustained brain growth during intrauterine life at the expense of growth of the trunk and abdominal viscera, a pattern of growth that has been shown to be associated with raised blood pressure and plasma fibrinogen concentrations, 2 risk factors for stroke. The men remained short in early childhood, possibly as a result of living with large numbers of other people in overcrowded homes, but they had high rates of growth in height in later childhood. Accelerated growth has been linked to the development of hypertension. In adult life, low income and low social class were associated with a further increase in risk of the disease.
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Acknowledgments |
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This study was funded in part by a program grant from the British Heart Foundation, the Jahnsson Foundation, Finska Läkaresällskapet, Orion Corporation Research Foundation, and the Finnish Foundation for Cardiovascular Research.
Received November 23, 1999; revision received January 6, 2000; accepted January 7, 2000.
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References |
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 J. W Rich-Edwards, K. Kleinman, K. B Michels, M. J Stampfer, J. E Manson, K. M Rexrode, E. N Hibert, and W. C Willett Longitudinal study of birth weight and adult body mass index in predicting risk of coronary heart disease and stroke in women BMJ, May 14, 2005; 330(7500): 1115. [Abstract] [Full Text] [PDF]
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 B. Galobardes, J. W. Lynch, and G. Davey Smith Childhood Socioeconomic Circumstances and Cause-specific Mortality in Adulthood: Systematic Review and Interpretation Epidemiol. Rev., July 1, 2004; 26(1): 7 - 21. [Full Text] [PDF]
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 J. P. Pell, G. C. S. Smith, and D. Walsh Pregnancy Complications and Subsequent Maternal Cerebrovascular Events: A Retrospective Cohort Study of 119,668 Births Am. J. Epidemiol., February 15, 2004; 159(4): 336 - 342. [Abstract] [Full Text] [PDF]
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D. J.P. Barker and D. T. Lackland Prenatal Influences on Stroke Mortality in England and Wales Stroke, July 1, 2003; 34(7): 1598 - 1602. [Abstract] [Full Text] [PDF]
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C L Hart and G Davey Smith Relation between number of siblings and adult mortality and stroke risk: 25 year follow up of men in the Collaborative study J. Epidemiol. Community Health, May 1, 2003; 57(5): 385 - 391. [Abstract] [Full Text] [PDF]
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E Hypponen, D A Leon, M G Kenward, and H Lithell Prenatal growth and risk of occlusive and haemorrhagic stroke in Swedish men and women born 1915-29: historical cohort study BMJ, November 3, 2001; 323(7320): 1033 - 1034. [Full Text] [PDF]
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P McCarron, C L Hart, D Hole, and G D. Smith The relation between adult height and haemorrhagic and ischaemic stroke in the Renfrew/Paisley study J. Epidemiol. Community Health, June 1, 2001; 55(6): 404 - 405. [Full Text] [PDF]
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