International Journal of HypertensionVolume 2011 (2011), Article ID 987159, 5 pagesdoi:10.4061/2011/987159

Research Article

The Association of Hypertension with Obesity and Metabolic Abnormalities among Chinese Children

Haiquan Xu,¹ Xiaoqi Hu,¹ Qian Zhang,¹ Songming Du,¹ Hongyun Fang,¹ Ying Li,² Jun Ma,³ Tingyu Li,⁴ Lin Du,⁵ Hongwei Guo,⁶ Guifa Xu,⁷ and Ailing Liu¹

¹National Institute for Nutrition and Food Safety, Chinese Center for Disease Control and Prevention, Beijing 100050, China²Haerbin Medical University, Heilongjiang, Haerbin 150081, China³Institute of Children and Adolescent Health, Peking University Health Science Center, Beijing 100191, China⁴Chongqing Children's Hospital, Chongqing 400014, China⁵Guangzhou Center for Disease Control and Prevention, Guangdong, Guangzhou 510515, China⁶School of Public Health, Fudan University, Shanghai 200032, China⁷Department of Public Health, Shandong University, Shandong, Jinan 250012, China

Received 3 August 2011; Revised 22 October 2011; Accepted 24 October 2011

Academic Editor: Claudio Borghi

Copyright © 2011 Haiquan Xu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

A total of 8898 Chinese children (4580 boys and 4318 girls) aged 7–13 years in 6 cities of east China were recruited. Data on height, weight, waist circumference, blood pressure, serum lipid profiles, glucose, and insulin were collected. The overall prevalence of hypertension was 11.1%. Overweight and obese children had a higher risk of developing hypertension than their counterparts (29.1%, 17.4%, and 7.8%, resp.) (). The means levels of triglycerides, glucose, insulin, and HOMA-IR (1.0 mmol/L, 4.5 mmol/L, 8.4 mU/mL and 1.7, resp.) among hypertensive children were all significantly higher than their normotensive counterparts (0.8 mmol/L, 4.5 mmol/L, 5.9 mU/mL, and 1.2, resp.) (). Compared with the healthy children, the risk (odds ratio, OR) of having hypertension among children with high triglycerides, hyperglycemia, and metabolic syndrome was 1.4 (95% confidence interval (CI): 1.0–2.0, ), 1.5 (95% CI: 0.9–2.5, ), and 2.8 (95%CI: 1.5–5.4, ), respectively, after controlling for age, gender, BMI, income level, parents' education level and puberty. In conclusion, overweight and obese children have higher risk of having hypertension and children with dyslipidemia, hyperglycemia, and metabolic syndrome and higher HOMA-IR have higher risk of developing hypertension.

1. Introduction

Hypertension is a major public health problem worldwide. In China, the prevalence of hypertension was 17.7% in 2002 and it was estimated that the number of adults with hypertension was 174 million and 220 thousands died from hypertension annually, respectively. About 2.54 million life years might be lost potentially due to hypertension. Every hypertensive patient led about 11.4 years life lost on average. Moreover, the direct economic burden reached 31.89 billion RMB [1]. It is well known that hypertension is one of the major risk factors for coronary artery disease and cerebrovascular disease [2, 3].

Development of adult hypertension and the adverse effects of elevated blood pressure on vascular structure and function may start very early in life [4–8]. Obesity is well known as one predictor of hypertension [9]. Some studies also showed the relationship between hypertension and cholesterol, glucose, insulin, and insulin resistance [10, 11]. However, these relationships appear to vary among ethnic groups [12]. The data on the relationship between hypertension and lipid profiles, glucose, insulin, and insulin resistance among Chinese children were limited. Therefore, the purpose of the present study was to explore the association of hypertension with obesity, metabolic abnormities including dyslipidemia, hyperglycemia, hyperinsulinemia, and metabolic syndrome among Chinese children.

2. Materials and Methods

2.1. Participants

Multi-stage randomly cluster sampling method was used to recruit participants. Firstly, six provincial capital cities in Eastern China, including Haerbin, Beijing, Jinan, Shanghai, Chongqing, and Guangzhou were selected for this study. From each city, 6 schools were then selected randomly. Lastly, 2 classes from each grade were selected randomly in 1st–5th grade of each school, and all students in the two classes were involved in the study. A total of 9866 children aged 7–13 years were recruited and 8898 participants (4580 boys and 4318 girls) gave both blood samples and physical measurements. The information on education and income level of the parents was collected from parents by using a questionnaire. The information on puberty was surveyed by the face to face inquiry to the participants.

The protocol of the survey was approved by the Ethical Committee of the National Institute for Nutrition and Food Safety, Chinese Center for Disease Control and Prevention. Signed consent forms were obtained from both the children’s parent(s) or guardian and the children themselves.

2.2. Anthropometric Measurements

Height was measured in bare feet to 0.1 cm with a freestanding stadiometer mounted on a rigid tripod (GMCS-I, Xindong Huateng Sports Equipment Co. Ltd., Beijing, China). Fasting body weight was measured to the nearest 0.1 kg on a double ruler scale (RGT-140, Wujin Hengqi Co. Ltd., Changzhou, China) with participants wearing lightweight clothing. BMI was calculated as weight in kilograms divided by height in meters squared (kg/m²). Using age- and sex-specific BMI cutoff points developed by the working group for obesity in China (WGOC), normal weight was defined as BMI for age and sex ≤85th percentile and overweight was defined as BMI between the 85th and the 95th percentiles, whereas obesity was defined as BMI ≥ 95th percentile [13]. Waist circumference (WC) was measured to the nearest 0.1 cm at the midway between the lower rib margin and the iliac crest with flexible anthropometric tape (Myotape). The WC was measured twice, and if the variation between these two measurements was greater than 2 cm, a third measurement was taken and the mean was calculated by using the two closest measurements. Height, weight, and WC were all objectively measured by trained investigators following standard procedures.

2.3. Blood Pressure and the Definition of Hypertension

Blood pressure was measured to the nearest 2 mmHg in the seated position using a mercury sphygmomanometer by trained nurses with at least a 10 min rest period before the measurement. The first and fifth Korotkoff sounds were used to represent the systolic (SBP) and diastolic blood pressure (DBP), respectively. Three measurements were taken from all the participants at 2 min intervals, and the average of the last two measurements was recorded. Hypertension was defined as SBP and/or DBP ≥95th age- and gender-specific percentile developed by Mi et al. for Chinese children and adolescents [14].

2.4. Serum Glucose, Insulin, and Lipid Profiles

Fasting blood sample (5 mL) of teach participant was collected in the morning after approximately 10–14 hours of overnight fasting. Serum glucose was determined by a glucose-oxidase method (Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan) within 4 hours after the fasting blood sample was obtained. Total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were determined by enzymatic methods using commercial kits (Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan). Serum insulin was determined by the AxSYM based on the microparticle enzyme immunoassay technology. The homeostatic index for insulin resistance (HOMA-IR) was calculated according to the homeostatic model as HOMA-IR = insulin fasting (μU/mL) × glycemia fasting (mmol/L)/22.5 [15, 16].

2.5. Definition of Metabolic Abnormalities

According to the International Diabetes Federation (IDF) definition [17]. Metabolic syndrome was diagnosed by abdominal obesity (≥90th percentile as assessed by WC with cutoff values from Chinese children [18]) and the presence of two or more clinical features including high triglycerides (TG ≥ 1.7 mmol/L), low HDL-C (HDL-C < 1.03 mmol/L), elevated blood pressure (SBP ≥ 130 mmHg or DBP ≥ 85 mmHg), and hyperglycemia (fasting glucose ≥ 5.6 mmol/L).

2.6. Statistical Analysis

The prevalence of hypertension was estimated overall by sex, age, and BMI. Prevalence values were compared using generalized linear mixed model (GLMMIX). Considering the complex study design, generalized linear mixed model was used to compare the fixed effect on the likelihood of hypertension after controlling for random effects. The fixed effects included sex, age, BMI status, income level, parents’ education level, and puberty, and the class was taken as random effect. The means of continuous variables were compared using mixed linear model (MIXED). All statistical analyses were done with SAS (9.2e for Windows; SAS Institute Inc. Cary, NC, USA), and the significance level was set at 0.05.

3. Results

The characteristics of the participants are shown in Table 1. Height, weight, BMI, and WC were higher among children with hypertension than children with normal blood pressure. Hypertensive children had a higher level of TG, glucose, insulin, and HOMA-IR than their normotensive counterparts after adjustment for age, gender, BMI, income level, parents’ education level, and puberty ().

Table 1: The characteristics of participants (mean ± SD).

Normotensive
Hypertensive
Total

Age (years)

0.0306

Height (cm)

<0.0001*

Weight (kg)

<0.0001*

WC (cm)

<0.0001*

BMI (kg/m²)

<0.0001*

TG (mmol/L)

<0.0022**

TC (mmol/L)

HDL-C (mmol/L)

LDL-C (mmol/L)

Glucose (mmol/L)

<0.0001**

Insulin (mU/mL)

<0.0001**

HOMA-IR

<0.0001**

* Adjusted for age, gender, income level, parents’ education level, and puberty.

** Adjusted for age, gender, BMI, income level, parents’ education level, and puberty.

The overall prevalence of hypertension among Chinese children was 11.1%. Compared with the normal-weight children, overweight and obese children had a higher risk for developing hypertension. The odds ratio (OR) was 2.9 (95% CI: 2.3–3.6) and 6.0 (95% CI: 4.9–7.4) for overweight and obese children, respectively. The prevalence of hypertension among abdominal obese children was higher than their counterparts (27.9% versus 8.4%, OR = 4.6, 95% CI: 3.8–5.5) (Table 2).

Table 2: The prevalence of hypertension in Chinese children by weight status.

N (%)
OR (95% CI)

Total ()
985 (11.1)
—
—

Weight status

    Normal weight ()
539 (7.8)
1
—

    Overweight ()
177 (17.4)
2.9 (2.3–3.6)
<0.0001

    Obesity ()
269 (29.1)
6.0 (4.9–7.4)
<0.0001

Abdominal obesity

     No ()
650 (8.4)
1
—

     Yes ()
335 (27.9)
4.6 (3.8–5.5)
<0.0001

Adjusted for age, gender, income level, parents’ education level, and puberty.

Compared with their counterparts, children with high triglycerides (OR = 1.4, 95% CI: 1.0–2.0, ), hyperglycemia (OR = 1.5, 95% CI: 0.9–2.5, ), low HDL-C (OR = 0.9, 95% CI: 0.6–1.2, ), and metabolic syndrome (OR = 2.8, 95% CI: 1.5–5.4, ) had a higher risk for having hypertension after controlling for the age, gender, and BMI. The prevalence of hypertension was higher at higher insulin and HOMA-IR values ( in each); the odds ratio was 1.6 (95% CI: 1.4–2.0) and 1.6 (95% CI: 1.4–2.0) after controlling for age, sex, BMI, income level, parents’ education level, and puberty, respectively (Table 3).

Table 3: The prevalence of hypertension among children with metabolic abnormalities and normal children.

No (%)
OR
Yes (%)
OR (95% CI)

High TG
10.6
1
23.3
1.4 (1.0–2.0)
0.0334

Low HDL-C
11.0
1
12.6
0.9 (0.6–1.2)
0.4507

Hyperglycemia
11.0
1
15.5
1.5 (0.9–2.5)
0.0890

MetS
10.8
1
51.9
2.8 (1.5–5.4)
0.0014

Insulin
7.7
1
16.6
1.6 (1.4–2.0)
<0.0001

HOMA-IR
7.5
1
15.4
1.6 (1.4–2.0)
<0.0001

Adjusted for age, gender, BMI, income level, parents’ education level, and puberty.

The cutoff point was median for insulin and HOMA-IR.

4. Discussion

Our study showed that the prevalence of hypertension increased with the weight status among Chinese children and the risk of having hypertension for obese children or abdominal obese children was higher than normal-weight children. These findings were consistent with previous studies in South Asian children [19, 20] and Caucasian children [21–23]. Obesity in childhood is one of the main predictors of hypertension in both childhood and adulthood [23]. Given the alarming increase in childhood obesity in China [24], the number of children with hypertension will increase rapidly.

The current study also indicated that, after controlling for age, gender, and BMI, the levels of TG and glucose among hypertensive children were higher than normotensive children. Hypertensive children were more likely to have higher TG, hyperglycemia, and MetS compared with their normotensive counterparts. These findings are consistent with the previous studies in Chinese adults [25, 26] and other ethnic populations [27–29]. TG increase may promote hypertension by the development of atherosclerotic changes in blood vessels [30]. Moreover, the pre-3-lipoprotein fraction rich in endogenous triglycerides inhibits the plasminogen activator secretion in the blood vessel wall and its deficiency may cause inhibition of fibrinolysis. The fibrinolysis inhibition also can promote hypertension by the development of atherosclerotic changes in blood vessels [30]. Hyperglycemia can alter intracellular signaling pathway leading to endothelial dysfunction, which was associated with increased blood pressure [31, 32].

Insulin and HOMA-OR in children with hypertension was found higher than children with normal blood pressure in our study. Some previous studies indicated the positive relationship between hyperinsulinemia, insulin resistance and hypertension and/or blood pressure [33, 34]. Insulin resistance might cause compensatory hyperinsulinemia, while hyperinsulinaemia could stimulate the activity of the sympathetic nervous system and kidney sodium and volume reabsorption, which could contribute to hypertension [35]. In addition, insulin resistance has been shown to be associated with impaired endothelium-dependent vasodilatation [36], which could contribute to increase blood pressure.

In conclusion, overweight and obese children were at a higher risk of having hypertension. Hypertensive children had a higher level of TG, glucose, insulin, and HOMA-IR. There is a higher risk of developing hypertension among children with dyslipidemia, hyperglycemia, and MetS than their counterparts. Effective interventions should be targeted for Chinese children at the onset of childhood obesity and hypertension.

Authors contribution

Y. Li, J. Ma, T. Li, L. Du, H. Guo, and G. Xu equally contributed to the paper.

Conflict of Interests

None of the authors had a personal or financial conflict of interests.

Acknowledgments

The authors would like to acknowledge the support from all the team members and local education and health staffs. They also appreciated all the participants and their parents for their participation. This project was funded by the China Ministry of Science and Technology as “Key Projects in the National Science & Technology Pillar Program during the Eleventh Five-Year Plan Period” (Grant no. 2008BAI58B05).

References

J. S. Wang, Y. Jiang, and S. G. Jin, “Burden of diseases contributed to hypertension in China,” Chinese Journal of Prevention and Control of Chronic Non-communicate Disease, vol. 15, no. 3, pp. 194–196, 2007.

U. N. Khot, M. B. Khot, C. T. Bajzer et al., “Prevalence of conventional risk factors in patients with coronary heart disease,” Journal of the American Medical Association, vol. 290, no. 7, pp. 898–904, 2003.

P. Magnus and R. Beaglehole, “The real contribution of the major risk factors to the coronary epidemics: time to end the "only-50%" myth,” Archives of Internal Medicine, vol. 161, no. 22, pp. 2657–2660, 2001.

C. L. Shear, G. L. Burke, D. S. Freedman, and G. S. Berenson, “Value of childhood blood pressure measurements and family history in predicting future blood pressure status: results from 8 years of follow-up in the Bogalusa Heart Study,” Pediatrics, vol. 77, no. 6, pp. 862–869, 1986.

J. R. Ingelfinger, “Pediatric antecedents of adult cardiovascular disease—awareness and intervention,” New England Journal of Medicine, vol. 350, no. 21, pp. 2123–2126, 2004.

S. D. Daniels, R. A. Meyer, and J. M. H. Loggie, “Determinants of cardiac involvement in children and adolescents with essential hypertension,” Circulation, vol. 82, no. 4, pp. 1243–1248, 1990.

C. Hanevold, J. Waller, S. Daniels, R. Portman, and J. Sorof, “The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the international pediatric hypertension association,” Pediatrics, vol. 113, no. 2, pp. 328–333, 2004.

P. H. Whincup, D. G. Cook, F. Adshead et al., “Cardiovascular risk factors in British children from towns with widely differing adult cardiovascular mortality,” British Medical Journal, vol. 313, no. 7049, pp. 79–84, 1996.

A. Chockalingam, “Healthy weight—healthy blood pressure,” Canadian Journal of Cardiology, vol. 26, no. 5, pp. 259–260, 2010.

E. Oda and R. Kawai, “LDL cholesterol is associated with blood pressure in Japanese women,” Diabetes Care, vol. 32, no. 9, p. e113, 2009.

A. R. Sinaiko, J. Steinberger, A. Moran, C. P. Hong, R. J. Prineas, and D. R. Jacobs Jr., “Influence of insulin resistance and body mass index at age 13 on systolic blood pressure, triglycerides, and high-density lipoprotein cholesterol at age 19,” Hypertension, vol. 48, no. 4, pp. 730–736, 2006.

M. F. Saad, S. Lillioja, B. L. Nyomba et al., “Racial differences in the relation between blood pressure and insulin resistance,” New England Journal of Medicine, vol. 324, no. 11, pp. 733–739, 1991.

G. S. Ma, C. Y. E. Ji, J. Ma et al., “Waist circumference reference values for screening cardiovascular risk factors in chinese children and adolescents,” Biomedical and Environmental Sciences, vol. 23, no. 1, pp. 21–31, 2010.

J. Mi, T. Wang, L. Meng, et al., “Development of blood pressure reference standards for Chinese children and adolescents,” The Chinese Journal of Evidence-Based Pediatrics, vol. 5, no. 1, pp. 4–14, 2010.

S. M. Haffner, H. Miettinen, and M. P. Stern, “The homeostasis model in the San Antonio Heart Study,” Diabetes Care, vol. 20, no. 7, pp. 1087–1092, 1997.

D. R. Matthews, J. P. Hosker, and A. S. Rudenski, “Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man,” Diabetologia, vol. 28, no. 7, pp. 412–419, 1985.

A. P. Ferreira, C. E. R. Oliveira, and N. M. França, “Metabolic syndrome and risk factors for cardiovascular disease in obese children: the relationship with insulin resistance (HOMA-IR),” Jornal de Pediatria, vol. 83, no. 1, pp. 21–26, 2007.

P. Zimmet, K. G. Alberti, F. Kaufman et al., “The metabolic syndrome in children and adolescents—an IDF consensus report,” Pediatric Diabetes, vol. 8, no. 5, pp. 299–306, 2007.

B. Mohan, N. Kumar, N. Aslam et al., “Prevalence of sustained hypertension and obesity in urban and rural school going children in Ludhiana,” Indian Heart Journal, vol. 56, no. 4, pp. 310–314, 2004.

N. K. Anand and L. Tandon, “Prevalence of hypertension in school going children,” Indian Pediatrics, vol. 33, no. 5, pp. 377–381, 1996.

Y. Ostchega, M. Carroll, R. J. Prineas, M. A. McDowell, T. Louis, and T. Tilert, “Trends of elevated blood pressure among children and adolescents: data from the National Health and Nutrition Examination Survey 1988–2006,” American Journal of Hypertension, vol. 22, no. 1, pp. 59–67, 2009.

Q. He, Z. Y. Ding, D. Y. T. Fong, and J. Karlberg, “Blood pressure is associated with body mass index in both normal and obese children,” Hypertension, vol. 36, no. 2, pp. 165–170, 2000.

H. M. Ippisch and S. R. Daniels, “Hypertension in overweight and obese children,” Progress in Pediatric Cardiology, vol. 25, no. 2, pp. 177–182, 2008.

Y. Li, E. G. Schouten, X. Hu, Z. Cui, D. Luan, and G. Ma, “Obesity prevalence and time trend among youngsters in China, 1982–2002,” Asia Pacific Journal of Clinical Nutrition, vol. 17, no. 1, pp. 131–137, 2008.

G. T. C. Ko, J. C. N. Chan, and C. S. Cockram, “Age, body mass index and 2-hour plasma glucose are the major determinants of blood pressure in Chinese women newly diagnosed to have glucose intolerance,” International Journal of Cardiology, vol. 69, no. 1, pp. 33–39, 1999.

Y. Ruixing, W. Jinzhen, L. Weixiong, C. Yuming, Y. Dezhai, and P. Shangling, “The environmental and genetic evidence for the association of hyperlipidemia and hypertension,” Journal of Hypertension, vol. 27, no. 2, pp. 251–258, 2009.

J. Klosi, O. Bare, M. Gjata, and M. Tase, “Prevalence of the metabolic syndrome in essential hypertension patients,” Journal of Hypertension, vol. 28, p. e580, 2010.

S. Bo, R. Gambino, L. Gentile et al., “High-normal blood pressure is associated with a cluster of cardiovascular and metabolic risk factors: a population-based study,” Journal of Hypertension, vol. 27, no. 1, pp. 102–108, 2009.

J. Papadakis, H. Mavrogeni, G. Vrentzos, M. Zeniodi, and E. Ganotakis, “Patients with essential hypertension have increased prevalence of metabolic syndrome,” Journal of Hypertension, vol. 28, p. e580, 2010.

F. Spöttl, F. Holzknecht, and H. Braunsteiner, “Inhibitors of the plasminogen-activation in patients with primary "carbohydrate-induced" hypertriglyceridemia,” Journal of atherosclerosis research, vol. 8, no. 5, pp. 821–826, 1968.

M. Lorenzi, J. A. Nordberg, and S. Toledo, “High glucose prolongs cell-cycle traversal of cultured human endothelial cells,” Diabetes, vol. 36, no. 11, pp. 1261–1267, 1987.

M. Lorenzi, D. F. Montisano, S. Toledo, and A. Barrieux, “High glucose induces DNA damage in cultured human endothelial cells,” Journal of Clinical Investigation, vol. 77, no. 1, pp. 322–325, 1986.

M. Modan, H. Halkin, S. Almog, et al., “Hyperinsulinemia. A link between hypertension obesity and glucose intolerance,” Journal of Clinical Investigation, vol. 75, no. 3, pp. 809–817, 1985.

C. P. Lucas, J. A. Estigarribia, L. L. Darga, and G. M. Reaven, “Insulin and blood pressure in obesity,” Hypertension, vol. 7, no. 5, pp. 702–706, 1985.

G. M. Reaven and B. B. Hoffman, “A role for insulin in the aetiology and course of hypertension?” The Lancet, vol. 2, no. 8556, pp. 435–436, 1987.

S. B. Wheatcroft, I. L. Williams, A. M. Shah, and M. T. Kearney, “Pathophysiological implications of insulin resistance on vascular endothelial function,” Diabetic Medicine, vol. 20, no. 4, pp. 255–268, 2003.