Evidence that fructose intake may modify blood pressure is generally limited to adult populations. This study examined cross-sectional associations between dietary intake of fructose, serum uric acid and blood pressure in 814 adolescents aged 13–15 years participating in the Western Australian Pregnancy Cohort (Raine) Study. Energy-adjusted fructose intake was derived from 3-day food records, serum uric acid concentration was assessed using fasting blood and resting blood pressure was determined using repeated oscillometric readings. In multivariate linear regression models, we did not see a significant association between fructose and blood pressure in boys or girls. In boys, fructose intake was independently associated with serum uric acid (P<0.01), and serum uric acid was independently associated with systolic blood pressure (P<0.01) and mean arterial pressure (P<0.001). Although there are independent associations, there is no direct relationship between fructose intake and blood pressure. Our data suggest that gender may influence these relationships in adolescence, with significant associations observed more frequently in boys than girls.
Hypertension is the most common disease of Western populations, and is becoming increasingly common in adolescents.1, 2 Between the 1988–1994 and 1999–2000 National Health and Nutrition Examination Survey (NHANES), systolic blood pressure (SBP) and diastolic blood pressure (DBP) significantly increased by 1.4 and 3.3 mm Hg, respectively, in American children and adolescents (aged 8–17 years).2 Hypertension in adolescence has been associated with an increased risk of early development of coronary artery disease and left ventricular hypertrophy, as well as numerous other conditions.3 Additionally, adolescent hypertension has been linked with an increased risk of hypertension and chronic disease in adulthood.4 Although the increasing trend in adolescent blood pressure (BP) has been largely attributed to increasing obesity, there are still unknown contributing factors.2 Dietary fructose is one of the potential risk factors currently under investigation in this regard.5, 6, 7
Fructose intake has been following an upward trend.8 In 2004, it was estimated that 9.1% of total energy intake for Americans was derived from fructose, an increase from the 8.1% estimate from 1978.9 Fructose is a monosaccharide naturally occurring in fruit and also commonly consumed as table sugar (sucrose) or high-fructose corn syrup.10 A study of 1999–2004 NHANES data estimated nonalcoholic beverages to contribute 46% of total fructose intake, followed by grain products at 17.3%.9 Several researchers have examined BP in relation to sugar-sweetened beverage intake in particular, because they are known to contribute a large proportion of fructose to Western diets.6, 11 Sugar-sweetened beverage intake was weakly but significantly related to greater SBP independent of obesity in a study of 4867 American adolescents by Nguyen et al.11 The authors suggested that elevated serum uric acid is part of a potential causal mechanism behind these findings. Studies of adult subjects also support the concept of a link between fructose and BP.5, 6, 7, 12
To our knowledge, the only published fructose data for adolescents to date are from the United States and Switzerland, and there are no published national statistics for fructose intake in Australia.9, 10, 13, 14 However, Woolley et al.15 recently collated a fructose database for adolescents involved in the 14-year follow-up of the Western Australian Pregnancy Cohort (Raine) Study. We have used these data in conjunction with BP measurements to conduct a cross-sectional analysis between fructose intake and BP in this group of Australian adolescents. We aimed to: (1) investigate the cross-sectional association between fructose intake and BP in adolescents participating in the Raine Study; (2) determine if fructose intake is associated with serum uric acid and if serum uric acid is associated with BP in adolescents; and (3) determine if serum uric acid is significant in the fructose–BP physiological pathway. We hypothesised that BP would be positively associated with fructose intake after adjustment for potential confounding factors, and that uric acid would be a significant factor in the physiological pathway.
Materials and methods
This cross-sectional study uses data from the 14-year follow-up of the Raine study.16 The study involves a large cohort, with dietary intake information, biochemical analyses, anthropometry and lifestyle data available.
The Raine Study began with 2900 women at 16–20 weeks of gestation who were involved in research evaluating the effects of ultrasounds in pregnancy. Women were recruited from King Edward Memorial Hospital (KEMH) in Perth and from private clinics. More detailed recruitment information has been published previously.16 The children born within the study were followed up at birth and at years 1, 2, 3, 5, 8, 10 and 14. There were 2868 live births, of which 1861 adolescents participated in at least one aspect of the 14-year follow-up. Of those who agreed to participate in the dietary assessment (n=1286), 962 completed and returned the required 3-day food diary and 822 produced usable diaries that were complete and representative of usual intake. Five were excluded because of use of medications known to affect BP and three did not have their BP measured, which reduced the subject number to 814 (419 boys and 395 girls). Consent for participation in the study was obtained from the subjects and their parents or guardians. Ethics were approved via the ethics committees of Princess Margaret Hospital and KEMH.
Assessment of dietary intake
A 3-day food diary in household measures was used to assess dietary intake. This is a validated tool for use in a younger population.17 Subjects who agreed to participate were provided with a food diary, metric spoons and cups and both written and verbal instructions. The food diaries were completed by the adolescents with parental assistance if required. The adolescents were asked to reflect whether each day of the food diary was an accurate representation of their usual diet. Unrepresentative food diaries were excluded from analysis. Additional information required was obtained by a dietitian via telephone in order to improve the accuracy of estimated intake.18
Records were entered into FoodWorks Professional Version 5 (Xyris Software Pty Ltd, Brisbane, Queensland, Australia, 2007), a dietary analysis programme used to analyse nutrient intake in the Australian population.19 As fructose values were not calculated by the software at the time of the study, intake was estimated for all foods containing 0.1 g of carbohydrate per 100 g or more with the aid of various nutrient databases.15 Fructose data were adjusted for total energy intake using the residuals method.20 Using energy-adjusted fructose intake takes into account the amount of fructose an adolescent is consuming in relation to energy intake. This helps to distinguish between adolescents who eat larger volumes of food and therefore have greater fructose intake as a result of overall higher intake, and those who are consuming a fructose-rich diet.
Assessment of physical and physiological characteristics
The adolescents underwent a physical assessment at the Telethon Institute of Child Health Research in Perth, Western Australia. Height was measured to the nearest 0.1 cm using a Holtain Stadiometer (Crymych, UK), and weight to the nearest 100 g using a Wedderburn Digital Chair Scale (Malaga, Western Australia, Australia). Adolescents were dressed in singlet tops and running shorts for both measurements. Body mass index (BMI) was calculated (weight (kg)/(height (m)2). BMI categories of underweight, normal weight, overweight and obese were defined using the Cole criteria for this age group.21, 22 A research assistant took waist measurements at the level of the umbilicus to the nearest 0.1 cm until two readings were within a centimetre of each other. The Tanner stages of pubic hair development scale was used to determine reproductive development stage of the adolescents via a privately completed questionnaire.23 Aerobic fitness, used to represent physical activity, was determined from the heart rate while on a bicycle ergometer using the Physical Work Capacity 170 protocol.24
A Dinamap ProCare 100 Monitor (General Electric Healthcare Technologies, Rydalmere, New South Wales, Australia) with appropriate cuff sizes was used to measure BP. Adolescents were rested for five minutes in a sitting position and BPs were determined from the last five readings taken over a period of 10 minutes. Mean arterial pressure (MAP) was calculated as DBP plus one-third of the pulse pressure. Fasting blood samples were analysed by the PathWest Laboratory at Royal Perth Hospital for uric acid using a Technicon Axon analyser and Technicon methods and reagents (Bayer Diagnostics, Leverkusen, Germany).
Subjects were categorised as having high BP if either their SBP or DBP was above age- and gender-specific adolescent definitions derived from the International Diabetes Federation (IDF) and the National Cholesterol Education Programme Adult Treatment Panel III (ATP).25
Sociodemographic and family characteristics
The carers of the adolescents were asked to report their education level, maternal age at conception, family income, family history of hypertension and whether the household was single or double parent. Maternal education level was categorised by the highest school year completed (grade 10 or less, grade 11 or grade 12). Maternal age at conception was also stratified (<20 years, 20–29 years or ⩾30 years). Family income, reported as gross annual Australian dollars, was divided into three groups: <$35 000, $35 000–70 000 or >$70 000. A positive history of family hypertension was recorded if a biological parent had been medically diagnosed.
Potential confounding factors
The potential confounding factors considered in this study included age, corrected gestational age, gender, birth weight, BMI, waist-to-height ratio, waist circumference, pubic hair development stage, family history of hypertension, level of maternal education, maternal age at birth, single-parent families, family income, energy intake, dietary sodium, dietary potassium, dietary fibre, dietary vitamin C, caffeine intake, alcohol intake, physical activity, screen time and aerobic fitness. Any supplementary vitamin C recorded in the food diary was included in the assessment of dietary vitamin C intake.
Predictive Analytics Software (PASW) for Windows, version 18.0 2009 (SPSS Inc., IBM, Chicago, IL, USA) was used for statistical analysis. Potential confounding factors were assessed for normality and were tested accordingly. Pearson’s correlation assessed normally distributed continuous variables. Spearman’s Rho correlation was used to assess skewed, continuous data. Independent t-tests assessed normally distributed variables with two categories and one-way analysis of variance (ANOVA) assessments were conducted for normally distributed variables with three or more categories. Significant confounding factors were then further assessed by multiple linear regression to determine their impact on the dependent variables (SBP, DBP, MAP and serum uric acid). Confounding factors that were not significant and did not contribute to improving the R2 value for the multiple linear regression models were removed.
Boys and girls were compared by independent t-tests for dietary, BP, uric acid or physical characteristic differences (mean±s.d. reported). Linear regression analyses that were unadjusted and multivariate linear regression analyses, adjusted for age and BMI and fully adjusted for confounding factors were used to analyse the relationships between energy-adjusted fructose intake and SBP, DBP, MAP and serum uric acid. For comparison, absolute fructose was assessed by multivariate linear regression using the full models, but with additional adjustment for energy intake. Multivariate linear regression also assessed the relationship between serum uric acid and BP variables using unadjusted, adjusted for age and BMI and fully adjusted models. As boys and girls had significantly different values for energy-adjusted fructose intake, serum uric acid, SBP and MAP, the multivariate linear regression analyses were conducted by gender. One-way ANOVA and χ2 analyses compared quartiles of energy-adjusted fructose intake and serum uric acid with BP variables. Confounders were considered significant at P<0.05.
The mean age of the adolescents included in this study was 14.2±0.2 years, ranging between 13.0 and 14.9 years. Descriptive data for anthropometric, BP and dietary intakes for the girls and boys are given in Table 1. Boys were significantly heavier and taller than girls, with higher energy intakes. Boys also had larger intakes of carbohydrate than girls; however, this difference was insignificant when adjusted for energy. Absolute fructose intake was higher in boys (P<0.01). When adjusted for energy, fructose intake was lower in boys than girls (P<0.01). The average intake for energy-adjusted fructose intake in the 95th percentile (top 5%) for the genders combined was 84.5 g. Fructose provided 9.2% of total energy intake in the group. There were no significant correlations determined between energy-adjusted fructose intake and weight (P=0.481) or BMI (P=0.991). Serum uric acid was significantly higher in boys when compared with girls. Systolic BP and MAP were lower in girls than boys (P<0.01). Diastolic BP was not significantly different between genders. The prevalence of high SBP and/or DBP in the group was 10.6% when defined using age- and gender-specific BP cut points.25
Fructose, serum uric acid and BP
Multivariate linear regression models examined energy-adjusted fructose intake with SBP, DBP, MAP and serum uric acid (Table 2). There were no significant associations between energy-adjusted fructose and the BP variables for either gender. Multivariate linear regression analyses for serum uric acid showed a positive association with energy-adjusted fructose for boys in an unadjusted model, a model adjusted for age and BMI only (partially adjusted) and a fully adjusted model. Assessment for girls showed a significant negative association in unadjusted and partially adjusted models, but not the fully adjusted model. Absolute fructose was assessed using the fully adjusted models but with the addition of energy intake as a confounding factor. Similar results were obtained for absolute fructose and uric acid with statistical significance observed in boys only (unstandardised β-coefficient 0.001; 95% confidence interval 0.0002–0.001; standardised β-coefficient 0.207; P<0.01).
Uric acid and BP
Multivariate linear regression models examined serum uric acid with SBP, DBP and MAP (Table 3). Boys showed significant relationships between serum uric acid and SBP in all three models (P<0.01) and MAP in unadjusted and fully adjusted models (P<0.01), with borderline significance when adjusted for age and BMI (P=0.053). An association was observed for girls between serum uric acid and SBP in an unadjusted model, but significance disappeared when confounding factors were considered.
Energy-adjusted fructose quartiles
Quartiles of energy-adjusted fructose intake were determined for girls and boys separately (Table 4). Assessment by one-way analysis of variance showed borderline significance for serum uric acid (P=0.052) in boys. However, post hoc testing showed no significant differences between energy-adjusted fructose quartiles for serum uric acid. Assessment by quartile also demonstrated associations for height, sodium, caffeine and vitamin C in boys, which were considered in the multivariate linear regression analyses. In girls, significance was observed for dietary sodium, caffeine and vitamin C, also accounted for in multivariate linear regression.
Serum uric acid quartiles
Assessment of energy-adjusted fructose intake and BP variables by quartiles of serum uric acid were conducted for both genders (Table 5). For boys, one-way ANOVA analyses showed that SBP and MAP were significantly different between quartiles of serum uric acid. Systolic BP and MAP increased in a step-wise manner with increasing serum uric acid. Boys in the highest quartile of serum uric acid had significantly higher SBP (P<0.0001) and MAP (P<0.05) than those in the lowest quartile of serum uric acid. One-way ANOVA demonstrated an association for SBP in girls, but no significance was demonstrated in post hoc testing between quartiles.
Relationship between fructose intake and BP
No direct relationships were shown between absolute or energy-adjusted fructose and SBP, DBP and MAP in boys or girls, which supports the null hypothesis. Several cross-sectional studies differ from our findings, reporting significant positive associations between fructose intake or sugar-sweetened beverage intake and BP.6, 7, 11 Points of difference include the use of 24-h food recalls in other studies, which may produce less representative results compared with 3-day food diaries,17 the measurement of fructose from sugar-sweetened beverages alone rather than from the whole diet, the smaller sample size of this study, differing nationalities, the assessment of genders combined rather than independently and the younger age of the Raine Study population.
Relationship between fructose and uric acid
A positive association was observed between absolute and energy-adjusted fructose and serum uric acid in boys. Assessment for girls showed a significant negative association in unadjusted and partially adjusted models, but not in fully adjusted models, which suggests that the result may be due to confounding. When boys were divided into quartiles of energy-adjusted fructose, the relationship was less distinct. Weakly but significantly greater uric acid concentrations and BP have been previously observed with greater intakes of sugar-sweetened beverage intake in 4867 American adolescents (P<0.05).11 However, gender was reported as an insignificant modifier for the relationship between sugar-sweetened beverage intake and serum uric acid.
The link we observed between fructose intake and serum uric acid in boys may be because of the way fructose is metabolised. Unlike glucose and galactose, fructose oxidation in the liver bypasses several regulatory stages. The liver therefore has less control over the flux of fructose through fructolysis, resulting in uric acid as a by-product.8
Relationships between serum uric acid and BP
Our study results showed positive associations between serum uric acid and SBP and MAP in boys, but not DBP. Analysis for girls showed significance in unadjusted models, but not the partially or fully adjusted models, suggesting that serum uric acid is not a significant independent predictor of BP in girls. In adolescents, serum uric acid has been related to both hypertension and metabolic syndrome.11, 26 A positive uric acid–BP association (SBP and DBP P<0.001) has been previously shown in adolescents with and without hypertension,27 and uric acid concentrations in childhood and adolescence have been shown to predict adult SBP and DBP (P<0.001).26 Elevated serum uric acid is also considered to be a potential risk factor for cardiovascular disease in the adult population.28
Results of rodent models and human studies suggest that the link between uric acid and BP is because of endothelial dysfunction resulting from a reduction in nitric oxide formation and pro-oxidant effects on endothelial cells.29, 30 Along with a response to this by the renin–angiotensin system,30 hyperuricaemia would result in vasoconstriction, thus leading to an elevation in BP. Adding strength to the association are studies that have shown that fructose-induced hypertension can be changed by manipulating uric acid concentrations.12, 31 In an uncontrolled study of healthy men, a high fructose diet for two weeks increased uric acid and BP, but subjects who were given allopurinol (a xanthine oxidase inhibitor preventing the formation of uric acid) did not experience a significant increase in uric acid or BP.12 Similarly, in hypertensive adolescents, allopurinol significantly reduced uric acid and BP over a 2-week period.31 These studies support the association observed in our study between uric acid and BP in boys.
Approximately 11% of our cohort was defined as having high BP according to adolescent age-specific criterion. Based on a similar criteria, our figure is slightly higher than the 7% of US adolescents aged 12 to 19 years reported in the NHANES as having high BP,32 which may be because of differences in age.
There is literature that may explain why our study found associations in boys only. One common theory is that sex hormones contribute to the differences in serum uric acid concentrations between males and females.33, 34 Serum uric acid concentrations increase in boys at the time of puberty, and also in postmenopausal women, further adding weight to the link between sex hormones and serum uric acid.33, 34 Several studies support this theory, and have found oestrogen is protective against excessive serum uric acid concentrations in women.33, 35 It is hypothesised that oestrogen increases uric acid excretion, resulting in reduced serum uric acid concentrations.36 Additionally, oestrogen may promote vasodilation.37 The adolescents from the current study were nearing the end of puberty, with a mean Tanner stage of four, the maximum stage being five.23 This suggests that hormone concentrations in the adolescents would be nearing adult levels. This could explain the lower serum uric acid and BP in the girls who may have been benefitting from protective oestrogen effects. A study of 6768 American adolescents aged 12–17 years reported a similar effect with a significant positive association between uric acid and BP in males but not females.38 Although a negative association was seen in girls in the partially adjusted model, the association was no longer significant in the fully adjusted model that accounted for additional confounding factors. This suggests that a true negative association is unlikely to be present.
Our results suggest that moderating fructose intake in adolescence, particularly for boys, may be beneficial in maintaining normal serum uric acid concentrations, which were independently associated with BP. In our population, beverages (excluding 100% fruit juice, milk and flavoured milks) were found to be the greatest contributors to fructose in the adolescents’ diets.15 Per capita, Australia ranks among the top 10 countries for soft drink consumption in the world.39 Sugar-sweetened carbonated beverages were the largest contributor at 62%, suggesting that reducing consumption of soft drinks and other sugar-sweetened beverages could be a potential strategy for decreasing fructose intake in adolescents. Fruit (excluding fruit juice) was the second largest contributor to fructose intake; however, fruit is nutrient dense and therefore fruit restriction is not recommended to reduce fructose consumption because of the health effects of fibre, potassium, vitamins and phytochemicals contained in fruit. It has previously been reported that socioeconomic characteristics were associated with food sources of fructose in our cohort.15 Adolescents who had older and more educated mothers consumed higher quantites of fructose from fruit, whereas consumption of fructose from beverages was higher in adolescents from families with lower incomes.15
Strengths and limitations
A strength of our study is the use of 3-day food diaries for the assessment of nutritional intake. The 3-day food diaries assess nutrient intake more accurately than 24-h recalls and have been validated in a younger population.17 However, 3-day food diaries can also be considered as limited as only 3 days are covered, and therefore some foods eaten on occasion may go unreported. Another strength of the study is the extensive assessment of fructose values by Woolley et al.15 that included 99.7% of foods consumed containing a minimum of 0.1 g of carbohydrate per 100 g. A limitation stems from the cross-sectional study design, as no cause–effect relationships can be determined, and we also acknowledge that some of the observed significant associations may be due to chance, owing to the large number of statistical tests performed in analysis. A further limitation is the lack of a robust measure of dietary sodium as 24-h urine collections were not conducted for this study. The adolescents who completed the 3-day food diaries did have similarities that may distinguish them from the general population of West Australian adolescents. They were more likely to have older mothers, higher family income or a lower BMI than the nonrespondents.40 This could limit generalisation of study findings, although the pregnant women involved in the Raine study were recruited from a public hospital (KEMH), and families who were involved in the study were more likely to be of middle to lower socioeconomic status initially.41
To our knowledge, this study provides the first investigation of relationships between fructose intake, uric acid and BP in Australian adolescents. No independent significant relationships were observed between absolute or energy-adjusted fructose and SBP, DBP and MAP in boys or girls, which supports the null hypothesis. However, our results showed that increased fructose intakes in boys aged 13–15 years are associated with increased serum uric acid concentrations, which could act independently to increase SBP and MAP. This association was not observed in adolescent girls, possibly because of the protective hormonal effects and smaller body size, contributing to lower average serum uric acid, SBP and MAP. Maintenance of a healthy adolescent BP is essential in reducing the risk of diseases such as early coronary heart disease.3 Adolescent hypertension has also been associated with hypertension in adulthood and the associated increased risks of chronic disease, such as the cardiovascular diseases.4 Our study adds to the limited body of evidence that investigates the relationship between increased fructose intake, serum uric acid and BP in adolescent populations. Longer-term research is required to determine the underlying mechanisms between fructose metabolism, uric acid and BP to enable a better understanding of the effects of altering fructose intake on the health status of adolescents.
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We extend our thanks to the Raine Study participants and their families, and also to the Raine Study team for data collection and cohort coordination. We also thank the Royal Perth Hospital laboratories. Core management funding for the Raine Study is provided by the University of Western Australia, Raine Medical Research Foundation at UWA, the Faculty of Medicine, Dentistry and Health Sciences at UWA, the Telethon Institute for Child Health Research, Women and Infants Research Foundation, the Telethon Institute for Child Health Research and Curtin University. Funding for the 14-year follow-up was provided by NH&MRC (CIA Sly; ID 211912), NH&MRC Programme Grant (CIA Stanley; ID 003209), the Telstra Research Foundation, the West Australian Health Promotion Foundation, the Australian Rotary Health Research Fund and the National Heart Foundation of Australia, Beyond Blue.
All authors have read and approved the submission of the manuscript; the manuscript has not been published and is not being considered for publication elsewhere, in whole or in part, in any language, except as an abstract.
The authors declare no conflict of interest.
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Cite this article
Bobridge, K., Haines, G., Mori, T. et al. Dietary fructose in relation to blood pressure and serum uric acid in adolescent boys and girls. J Hum Hypertens 27, 217–224 (2013). https://doi.org/10.1038/jhh.2012.36
- blood pressure
- uric acid
- Raine Study
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