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Earlier epidemiologic studies have yielded inconsistent results on the extent and timing of the blood pressure (BP) increase in offspring of hypertensive parents. We hypothesized that a familial influence on the BP of the offspring exists from birth on, but becomes significant only later in childhood. We studied the influence of familial occurrence of hypertension on the BP of 3596 children aged 6 to 18 years during a 6-year follow-up. In addition, we examined the possible associations of BP variations with polymorphisms of two candidate genes for hypertension, ie, those coding for the angiotensin converting enzyme (ACE) and those coding for angiotensinogen. A positive family history of hypertension was reflected as the occurrence of higher systolic BP values from the age of 9 years and upward among the females and from the age of 12 years and upward among the males. The mean differences in BP varied from 3.2 to 5.8 mm Hg (systolic) and 2.1 to 5.9 mm Hg (diastolic) between the female offspring of normotensive and hypertensive parents and grandparents. The systolic BP values were significantly higher among females with a hypertensive history in two generations in comparison with females from normotensive families. Among the male offspring of hypertensive and normotensive families, the BP differences were inconsistent. The deletion/deletion males had higher systolic BP values than those with other ACE genotypes. In contrast, variation at the angiotensinogen gene locus was not significantly associated with BP. We conclude that parental history of hypertension is a risk factor for high blood pressure among the offspring from the ages of 9 to 12 years and upward, and hypertension within two generations may enhance this effect. Although the common genetic variation of ACE may influence blood pressure in male children and adolescents, our data do not suggest a role for the common variation of the angiotensinogen gene as a BP regulator during childhood.

Contradictory results have been published about the relation between copper, zinc and selenium and blood pressure (BP). To evaluate the role of these trace elements in BP regulation, we analysed the correlations between BP and copper, zinc and selenium, measured from serum, diet and hair among 3596 healthy children in a 6-year follow up. Fasting blood samples were used in serum copper, zinc and selenium analyses. The dietary intake of trace elements and energy were determined by the 48-h recall method. The hair copper and zinc analyses were performed from the naturally coloured hair samples. Correlation analysis was used to show the relation between BP and copper, zinc or selenium in each study year and during a 3- or 6-year follow-up period. The zinc-to-copper ratio in serum, diet and hair was calculated. In the correlation analyses the data was adjusted for weight and the daily intake of energy. Neither serum and diet copper or zinc, nor the zinc-to-copper ratio correlated uniformly with BP measured in the same year (correlation coefficients varying from -0.12 to 0.18) or in the subsequent years. Hair copper and zinc correlated weakly negatively with BP (correlation coefficients varying from -0.17 to -0.01). Serum selenium correlated weakly positively with systolic and diastolic BP measured in the same year (correlation coefficients varying from 0.03 to 0.14), but not with subsequent BP measured in the second or third survey. Dietary selenium had an inconsistent effect on BP (correlation coefficients varying from -0.14 to 0.26). In conclusion, copper, zinc, their ratio or selenium did not associate with BP, nor did they have any effect on subsequent BP.

To examine the levels and relationship of blood pressure and insulin during puberty, blood pressure and serum insulin were measured in 3596 subjects, aged 3-18 y, whose pubertal status was graded according to the Tanner classification. The same study protocol was repeated in two follow-up surveys 3 and 6 y later for 2991 6-21-y-old subjects and 2799 9-24-y-old subjects, respectively. There was a 37-66% increase in insulin at Tanner stage 3 (pubic hair) among the female subjects and at Tanner stage 5 (pubic hair) among the male subjects, after which insulin started to decrease. The mean systolic and diastolic blood pressure increased steadily throughout puberty. The rise in blood pressure continued during early adulthood, despite the decrease in serum insulin. The correlation between systolic blood pressure and insulin measured in the same year was weak at each pubertal stage after standardization for weight, except among the female subjects at mid puberty. There was no relation between diastolic blood pressure and insulin. Adult systolic blood pressure could be predicted by pubertal insulin among the male subjects after adjustment for age and weight (partial correlation coefficient 0.21), but among the female subjects this relation was trivial (partial correlation coefficient 0.08). We conclude that the correlation between insulin and actual blood pressure vanishes during puberty, whereas pubertal insulin and future adult male systolic blood pressure seem to correlate.

A negative correlation between birth weight and subsequent blood pressure has been reported, but in some studies this correlation has not been found. We analyzed the effect of birth weight and pubertal development and several pre- and postnatal factors on subsequent blood pressure among 2500 children and adolescents in a follow-up study with three surveys conducted with 3-y intervals. The correlations between birth weight and systolic blood pressure varied from -0.04 to 0.02 among the female subjects and from -0.05 to -0.04 among the male subjects in each survey. A somewhat stronger relation was found among the postpubertal female and male subjects (correlation coefficient -0.09 and -0.05) in the last survey. When adjusted for weight, the correlations became negative and more often significant. The decrease in the adjusted mean systolic blood pressure was about 2 mm Hg when birth weight increased from the lowest to the highest tertile. Other factors affecting systolic blood pressure were current age (mean change up to 1.8 mm Hg/ y) and weight (mean change up to 1.2 mm Hg/kg), the duration of breast feeding over 3 mo (mean change up to -6.5 mm Hg), and a birth rank order over four (mean change up to 5.0 mm Hg) presented as the mean difference from the baseline. According to the multiple regression analysis, a history of mother's high blood pressure during pregnancy (p < 0.05) predicted future blood pressure more eminently than birth weight. In conclusion, our results based on healthy children and adolescents offer support for the theory of low birth weight as a predicting factor for future blood pressure. However, other pre- and postnatal factors seem to be important as well.

Meta-analysis of blood pressure (BP) studies in children was performed in order to evaluate whether BP readings obtained in various studies may be pooled. In total 30 original reports on BP in children were analyzed and the age and sex-specific BP values reported for 12 and 15-year-old subjects in 11 of these were tested for homogeneity. The differences in sample size-weighted means between the devices used (with 95% confidence intervals) were evaluated. The BP values reported in different studies for systolic Korotkoffs first phase BP (K1) and diastolic Korotkoffs fourth (K4) and fifth (K5) phase BP were shown to be too heterogeneous (p < 0.001) to be pooled. Heterogeneity and measurement biases in the BP results were caused by differences between the devices and the diastolic BP indicator (K4 vs K5) and by observer biases such as uncontrolled terminal digit preference. The device-specific weighted means for K1, K4 and K5 BP in 12 and 15-year-old subjects showed statistically significant differences between random zero (RZS) and ordinary mercury (OMS) sphygmomanometer (p < 0.001) the difference (OMS-RZS) being from 0.7 to 6.6 mmHg for K1 (p < 0.001, except in 12-year-old girls), from 1.1 to 7.1 mmHg for K4 (p < 0.001, except in 12-year-old girls) and from 4.5 to 7.9 mmHg for K5 (p < 0.001). Such a discrepancy was also apparent between ordinary and automated mercury sphygmomanometer (AMS) in the case of diastolic K4 and K5 BP (p < 0.001), but not in K1. BP results obtained in different investigations using different BP devices and Korotkoffs phases as indicator of diastolic BP should not be pooled. More widely accepted recommendations are needed to standardize the measurement of BP in children.

We evaluated the role of insulin in regulating and predicting blood pressure among 3596 to 2799 Finnish children and adolescents aged 3 to 18 years who were followed from 1980 to 1986. Blood pressure, weight, and height were measured in three surveys 3 years apart. Fasting blood samples were drawn and serum insulin was analyzed. The effect of insulin on blood pressure was evaluated in each of the 3 study years, together with the effect of fasting insulin on future blood pressure and the effect of insulin on the change in blood pressure. We also analyzed the correlation between insulin and blood pressure in different age groups and the correlation between change in insulin and change in blood pressure. A constant positive correlation was found between insulin and both systolic and diastolic (Korotkoff's fifth phase) blood pressures measured in the respective years (correlation coefficients 0.10 to 0.41 and partial correlation coefficients 0.02 to 0.15), except between insulin and diastolic blood pressure in the first two surveys in terms of partial correlation and multiple regression analysis. Similarly insulin and blood pressure correlated positively in every age group. Insulin measured in 1980 or 1983 predicted systolic blood pressure as measured 3 and 6 years later (correlation coefficients 0.30 to 0.47 and partial correlation coefficients 0.06 to 0.13), and likewise diastolic blood pressure as measured 3 and 6 years later (correlation coefficients 0.17 to 0.35 and partial correlation coefficients 0.05 to 0.08), except among the males in 1983. Correlation between insulin and the change in blood pressure was not significant or remained marginal. Similarly, the correlation between change in insulin and change in blood pressure was not significant or remained marginal. We suggest that insulin seems to regulate actual blood pressure within the normal range and to predict future blood pressure among children and adolescents, independently of age and weight. However, insulin does not enhance the rise in blood pressure.

In adults hyperinsulinaemia is associated with an atherogenic risk profile including obesity, low levels of HDL-cholesterol, high levels of triglycerides and elevated blood pressure. To examine these associations in the young we studied the cross-sectional relationships of insulin with obesity indices (body mass index, subscapular skinfold thickness), serum lipids and blood pressure in 1,865 children, adolescents and young adults aged 6-24 years. We also used longitudinal data to study the value of a single insulin measurement to predict high risk factor levels and clustering of multiple risk factors after a 6-year follow-up. In cross-sectional analyses the levels of triglycerides, HDL-cholesterol, systolic blood pressure and obesity indices were usually significantly different across the quartiles of fasting insulin in both sexes among children, adolescents and young adults. In general, no associations were seen with total cholesterol or LDL-cholesterol. In prospective analysis elevated baseline insulin was related to the incidence of hypertriglyceridaemia (> or = 95th percentile) at the follow-up. This relationship persisted even after adjustments for baseline obesity or 6-year change in obesity status. Moreover, baseline insulin concentration was higher in subjects who subsequently showed clustering of high triglycerides, low HDL-cholesterol and high systolic blood pressure levels at the follow-up. We conclude that high fasting insulin levels measured in children and adolescents predict the development of hypertriglyceridaemia years later. In addition, high insulin levels seem to precede the development of a potentially atherogenic risk factor profile including low HDL-cholesterol, high triglycerides and high systolic blood pressure.

Controversy exists over the value of measuring diastolic blood pressure (BP) in children, and over whether this should be measured at Korotkoff's fourth phase (K4) or fifth phase (K5) of pulse sounds. We measured diastolic BP in 3012 randomly selected Finnish children aged 6-18 years in 1980, and in 2885 of the same individuals in 1983 and 2500 in 1986. BP was measured with a standard mercury sphygmomanometer in 1980 and 1983, and with a random-zero sphygmomanometer in 1986. K4 was consistently absent in 187 individuals (3.2%) in 1980 and 1983, and in 155 individuals (6.2%) in 1986. K5 was absent in only 34 individuals (0.6%) in 1980/83 and 5 (0.2%) in 1986. The difference between mean K4 and K5 diastolic BP varied from 6.5 to 9.2 mm Hg depending upon age. K4 and K5 BPs showed good correlation in all age groups. Reliable and repeatable BP measurements in all age groups of children are best achieved with K5 as the indicator of diastolic BP.

The question of whether blood pressure is one of the main risk factors for cardiovascular diseases in childhood has been evaluated in a Study of Cardiovascular Risk in Young Finns. In the second follow-up study, carried out in 1986, blood pressure was successfully measured in 2500 individuals aged nine to 24 years using a random zero sphygmomanometer. The mean systolic blood pressure in girls rose from 102 mmHg (95th percentile 119 mmHg) at age nine to 116 mmHg (138 mmHg) at age 24 and that in boys from 102 mmHg (95th percentile 121 mmHg) to 128 mmHg (148 mmHg). Diastolic blood pressure was more often measurable using Korotkoff's 5th than the 4th phase. The values observed were similar to those reported by the Second Task Force on Blood Pressure Control in Children, but owing to differences in the methods used to measure blood pressure it cannot be reliably concluded that the blood pressures were similar in the two series. Even in childhood blood pressure measurement is important, and since it changes with the physical size of the child, observations should be compared with normal values such as those reported here. No data are yet available to suggest that children with blood pressure values in the high normal range would benefit from interventions. Thus normal blood pressure value curves should be applied with caution when assessing children.

In connection with the Finnish Multicentre Study on the precursors of atherosclerosis in 3-, 6-, 9-, 12-, 15- and 18-year-old children and adolescents, blood pressure was measured in 3,596 subjects in the five university hospital areas. Blood pressure was measured with an ultrasound device (Arteriosonde 1020, Roche) in the 3-year-old children, and an ordinary mercury sphygmomanometer was used in the rest of the subjects. The systolic and diastolic values increased with age as has been shown earlier. There were no significant differences in the values between boys and girls except that the 15- and 18-year-old boys had values a little higher than girls of the same age. Weight and height correlated well to both systolic and diastolic blood pressures. Physical maturation also correlated to blood pressure.

Changes in blood pressure during the first year of life were investigated in a one-year follow-up study. The blood pressures were measured at the age of one day from 245 newborns, at the age of four or five days from 224 infants, at the age of four months from 105 infants, and at the age of one year from 68 infants. Blood pressure increased considerably during the first five days. The increase of mean systolic blood pressure was markedly bigger, from 59 to 90 mmHg, than that of mean diastolic blood pressure, which was from 43 to 55 mmHg. The correlations of blood pressure were calculated with prenatal history, physical measurements and parental blood pressure. Significant correlations were found with physical factors but not with the prenatal history or parental blood pressure. The tracking of the blood pressure was not good. The distribution of the blood pressure values was normal. It is concluded that for the time being there are no reliable predictive factors to hypertension which could be found in early infancy.