Utility of Waist-To-Height Ratio in Detecting Central Obesity and Related Adverse Cardiovascular Risk Profile Among Normal Weight Younger Adults (from the Bogalusa Heart Study)
Article Outline
Data on the utility of the waist-to-height ratio in detecting central obesity and related cardiovascular risk among normal weight younger adults are scant. This aspect was examined in 639 normal weight (body mass index 18.5 to 24.9 kg/m2) black and white adults (75% white and 36% men) 20 to 44 years old. The subjects with a waist-to-height ratio ≥0.5 were grouped as having central obesity normal weight, with the rest considered the control group. The subjects with central obesity, compared to the controls, after adjusting for age, race, and gender, had significantly greater diastolic blood pressure, mean arterial pressure, low-density lipoprotein cholesterol level, triglycerides, triglycerides/high-density lipoprotein cholesterol ratio, insulin, homeostasis model assessment of insulin resistance, uric acid, C-reactive protein, and liver function enzymes (alanine aminotransferase and γ-glutamyl transferase). On multivariate analysis, the central obesity group compared to the control group was 1.9, 2.2, 2.9, and 2.5 times more likely to have significantly adverse levels (top tertile vs the rest) of mean arterial pressure, triglycerides/high-density lipoprotein cholesterol ratio, homeostasis model assessment of insulin resistance, and C-reactive protein, respectively. The central obesity group also had a greater prevalence of dyslipidemia, hypertension, insulin resistance, hyperuricemia, and elevated C-reactive protein. The age-, race-, and gender-adjusted mean value of the common carotid intima-media thickness, a measure of subclinical atherosclerosis, was greater in the central obesity group compared to the control group (0.76 vs 0.71 mm, p = 0.009). In conclusion, these findings underscore the utility of the waist-to-height ratio in detecting central obesity and related adverse cardiovascular risk among normal weight younger adults.
The Framingham study and, subsequently, other studies have used the waist-to-height ratio as an easily measurable anthropometric index for routine evaluation of the association between central intra-abdominal adiposity and cardiometabolic risk.1, 2, 3 Although waist circumference has been advocated as an indicator of abdominal fat content, unlike the waist-to-height ratio, the cutpoints have varied by race, gender, and country.2, 4 However, information is scant regarding the utility of the waist-to-height ratio in detecting central obesity and related adverse cardiovascular risk among normal weight United States asymptomatic younger adults. The present study examined this aspect in the Bogalusa Heart Study cohort for whom cardiometabolic risk factor data and ultrasound measurement of the carotid intima-media thickness were available.
Methods
The Bogalusa Heart Study is a biracial (65% white, 35% black) community-based study of the natural history of cardiovascular disease since childhood.5 The present study sample was derived from a cohort of 2,065 subjects (70% white and 42% men) 20 to 44 years old who were examined as a part of a longitudinal follow-up survey. The participants (n = 639) with a body mass index of 18.5 to 24.9 kg/m2 were considered of normal weight and included in the present study. Using the previously recommended cutpoint,2 the study subjects with a waist-to-height ratio ≥0.5 were included in the central obesity normal weight group (n = 65), with the rest in the control group (n = 574). The institutional review board of the Tulane University Health Sciences Center approved the present study, and all participants gave informed consent.
Standardized protocols were used by trained examiners. The participants were instructed to fast overnight before the screening. Information on personal health and medication history was obtained by questionnaires. Anthropometric and blood pressure measurements were made in replicate, and the mean values were used in the analyses. The body mass index was evaluated as the weight in kilograms divided by the square of the height in meters. The mean arterial pressure was calculated as the diastolic blood pressure plus 1/3 of the pulse pressure.
The cholesterol and triglyceride levels in the serum were analyzed using enzymatic procedures on the Hitachi 902 Automatic Analyzer (Roche Diagnostics, Indianapolis, Indiana). Serum lipoprotein cholesterol levels were analyzed using a combination of heparin-calcium precipitation and agar-agarose gel electrophoresis procedures.6 A commercial radioimmunoassay kit was used to measure the plasma immunoreactive insulin levels (Phadebas, Pharmacia Diagnostics, Piscataway, New Jersey). Plasma glucose, uric acid, alanine aminotransferase, and γ-glutamyl transferase levels were measured as a part of a multiple chemistry profile (SMA 20) by enzymatic procedures with the multichannel Olympus Au-5000 analyzer (Olympus, Lake Success, New York). Plasma high-sensitivity C-reactive protein (CRP) was measured using a latex particle-enhanced immunoturbidimetric assay. Insulin resistance status was assessed using homeostasis model assessment of insulin resistance (HOMA-IR) according to the formula7: insulin (μU/ml) × glucose (mmol/L)/22.5.
Hypertension was defined as systolic blood pressure ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or the use of antihypertensive medication. Dyslipidemia was defined as low-density lipoprotein cholesterol ≥160 mg/dl, high-density lipoprotein (HDL) cholesterol <40 mg/dl, triglycerides ≥200 mg/dl, triglycerides/HDL cholesterol ratio ≥3.5, or the use of medication for these conditions. Insulin resistance was defined by a HOMA-IR value of >1.69.8 A triglyceride/HDL cholesterol ratio of ≥3.5 is also known to indicate insulin resistance.9 The cutpoint for an adverse level of uric acid and CRP was ≥6.5 mg/dl and ≥1.5 mg/L, respectively.
Images of the right and left common carotid segment were recorded using a Toshiba Sonolayer SSH 160 A (Toshiba Medical, Tokyo, Japan) ultrasound system and a 7.5-MHz linear array transducer according to the protocol developed for the Atherosclerosis Risk in Communities Study.10 Maximum intima-media thickness readings of the right and left far walls were averaged and used in the analyses. If bilateral images were not available, the value of 1 side was used as the mean.
All data analyses were performed using Statistical Analysis Systems, version 9.1 (SAS Institute, Cary, North Carolina). Differences in the mean values of the cardiometabolic risk factors between the central obesity normal weight and control groups were tested by analysis of covariance, adjusting for age, race, and gender. Differences in the percentages of the categorical variables were tested using the chi-square test. Insulin, HOMA-IR, triglycerides, and the triglyceride/HDL cholesterol ratio were log-transformed to improve the normality of the distribution in the analyses of covariance. The independent associations between central obesity and cardiometabolic risk factors were examined using a multivariate logistic regression analysis model, using central obesity (yes/no) as the dependent variable. Adverse levels of the risk factors were defined as the top tertile specific for age, race, and gender, and the remaining 2 tertiles were used as the reference group. The purpose of the present study was to examine a cross-sectional relation between central obesity and the risk factors instead of the causality. Therefore, using central obesity as a dependent variable in the logistic regression analysis was not meant to imply a cause-effect relation.
Results
As listed in Table 1, the normal weight subjects (n = 639) constituted 30.9% of the total cohort. Of these, 65 normal weight subjects (10.2%) had central obesity (waist-to-height ratio ≥0.5). The central obesity normal weight group, in addition to being relatively older, had significantly more men than women, and, after adjusting for age, race, and gender, had greater levels of diastolic blood pressure, mean arterial pressure, low-density lipoprotein cholesterol, triglycerides, triglycerides/HDL cholesterol ratio, insulin, HOMA-IR, uric acid, CRP, and liver function enzymes (γ-glutamyl transferase and alanine aminotransferase) than the control group.
Table 1. Demographic and cardiometabolic risk factors in normal weight (body mass index 18.5 to 24.9 kg/m2) young adults by waist-to-height ratio: the Bogalusa Heart Study
| Variable | Waist-to-Height Ratio | p Value⁎ | |
|---|---|---|---|
| <0.5 (n = 574) | ≥0.5 (n = 65) | ||
| Age (years) | 32.2 ±6.3 | 34.7±5.7 | 0.004 |
| Men (%) | 33.6% | 53.8% | 0.001 |
| White (%) | 75.0% | 76.9% | 0.728 |
| Systolic blood pressure (mm Hg) | 110±11 | 114±13 | 0.136 |
| Diastolic blood pressure (mm Hg) | 67±9 | 71±10 | 0.033 |
| Mean arterial pressure (mm Hg) | 85±9 | 90±11 | 0.036 |
| Low-density lipoprotein cholesterol (mg/dl) | 110±31 | 122±30 | 0.012 |
| High-density lipoprotein cholesterol (mg/dl) | 54±15 | 49±14 | 0.067 |
| Triglycerides (mg/dl) | 89±49 | 128±83 | <0.001† |
| Triglyceride/high-density lipoprotein cholesterol ratio | 1.9±1.3 | 2.9±2.3 | <0.001† |
| Glucose (mg/dl) | 79±14 | 82±10 | 0.191 |
| Insulin (μU/ml) | 7.6±4.3 | 10.0±4.4 | <0.001† |
| Insulin resistance index (HOMA-IR) | 1.5±1.2 | 2.0±0.9 | <0.001† |
| Uric acid (mg/dl) | 4.2±1.3 | 4.9±1.5 | 0.038 |
| C-reactive protein (mg/L) | 1.9±2.9 | 3.0±3.6 | 0.006 |
| γ-Glutamyl transferase (IU/L) | 24±23 | 35±31 | 0.010 |
| Alanine aminotransferase (IU/L) | 19±16 | 26±19 | 0.040 |
⁎Continuous variables (except for age) adjusted for age, race, and gender. |
†Derived using log-transformed scales. |
The results of the multivariate logistic regression analysis showing the odds of the central obesity normal weight group versus the reference control group (odds ratio 1.0) having adverse levels (top tertile vs the rest) of the risk factors are listed in Table 2. The independent variables included in the model are listed in Table 2. After adjusting for age, race, and gender, the central obesity normal weight group was 1.9, 2.2, 2.9, and 2.5 times more likely than the control group to have significantly elevated levels of mean arterial pressure, triglyceride/HDL cholesterol ratio, HOMA-IR, and CRP, respectively.
Table 2. Odds ratios and 95% confidence intervals for adverse levels of cardiometabolic risk factors in central obesity normal weight young adults: Bogalusa Heart Study
| Independent Variable (Top Tertile vs Rest)⁎ | OR | 95% CI | p Value |
|---|---|---|---|
| Mean arterial pressure | 1.91 | 1.09–3.35 | 0.025 |
| Low-density lipoprotein cholesterol | 1.58 | 0.89–2.80 | 0.117 |
| Triglyceride/high-density lipoprotein cholesterol ratio | 2.17 | 1.21–3.87 | 0.009 |
| Insulin resistance index (HOMA-IR) | 2.88 | 1.63–5.08 | <0.001 |
| C-reactive protein | 2.46 | 1.33–4.55 | 0.004 |
| Uric acid | 1.01 | 0.56–1.80 | 0.983 |
| Γ-Glutamyl transferase | 1.03 | 0.56–1.88 | 0.935 |
| Alanine aminotransferase | 1.72 | 0.95–3.12 | 0.076 |
⁎Adjusted for age, race, and gender; group with waist-to-height ratio <0.5 used as reference; all these variables were included in model. |
As listed in Table 3, the prevalence of cardiometabolic risk factors in the central obesity normal weight group was significantly greater with respect to hypertriglyceridemia, an elevated triglyceride/HDL cholesterol ratio, hypertension, elevated HOMA-IR, hyperuricemia, and elevated CRP compared to the control group.
Table 3. Prevalence of cardiometabolic risk factors in normal weight (body mass index 18.5 [%] to 24.9 kg/m2) young adults by waist-to-height ratio: the Bogalusa Heart Study
| Risk Factor⁎ | Waist-to-Height Ratio | p Value | |
|---|---|---|---|
| <0.5 | ≥0.5 | ||
| Dyslipidemia | |||
| Low-density lipoprotein cholesterol (≥160 mg/dl) | 7.0 | 9.2 | 0.506 |
| High-density lipoprotein cholesterol (<40 mg/dl) | 14.3 | 23.1 | 0.061 |
| Triglycerides ≥200 (mg/dl) | 3.8 | 13.9 | 0.000 |
| Triglyceride/high-density lipoprotein cholesterol ratio ≥3.5 | 8.7 | 20.0 | 0.004 |
| Hypertension (140/90 mm Hg) | 5.2 | 15.4 | 0.001 |
| Insulin resistance index (HOMA-IR) ≥1.69 | 25.8 | 57.8 | <0.001 |
| Hyperglycemia (glucose ≥100 mg/dl) | 1.4 | 4.7 | 0.063 |
| Hyperuricemia (uric acid ≥6.5 mg/dl) | 5.4 | 13.9 | 0.008 |
| Elevated C-reactive protein ≥1.5 mg/L | 30.1 | 52.0 | 0.002 |
⁎Prevalence included those taking medication for the condition. |
Figure 1 illustrates the age-, race-, and gender-adjusted mean level of common carotid intima-media thickness in the central obesity normal weight group versus the control group, with the former showing a greater value than the latter (0.76 vs 0.71 mm, p = 0.009).
Figure 1.
Common carotid intima-media thickness among normal weight (body mass index 18.5 to 24.9 kg/m2) younger adults by waist-to-height ratio (<0.5 vs ≥0.5): the Bogalusa Heart Study.
Discussion
The present community-based study used the waist-to-height ratio as a simple anthropometric measure of central (visceral) obesity in normal weight persons and found that normal weight subjects with central obesity were characterized by an increased mean arterial pressure, triglyceride/HDL cholesterol ratio, insulin resistance as shown by the HOMA-IR, and CRP compared to normal weight persons without central obesity. In addition, they had an excess carotid intima-media thickness, a validated marker of subclinical atherosclerosis.11, 12 These observations are in accordance with the emerging concept of subgroups of obesity and their phenotypic characteristics in terms of constellations of cardiometabolic risk factors related to cardiovascular disease.13, 14, 15, 16
The present finding that the mean arterial pressure, triglyceride/HDL cholesterol ratio, HOMA-IR, and CRP are independent correlates of central obesity normal weight status is in accordance with the interrelated pathophysiologic traits of central adiposity, collectively recognized as the metabolic syndrome.17, 18, 19 As a highly active endocrine organ, excess central (visceral) adiposity plays an important role in the dysregulation of hemodynamic, metabolic, and inflammatory processes through mechanisms that include, among others, activation of release of free fatty acids from the adipocytes, macrophage infiltration into the adipose tissue, hepatic insulin resistance, hepatic lipogenesis, adipose renin-angiotensin-aldosterone system, sympathetic nervous system, proinflammatory cytokines (tumor necrosis factor-α and interleukin-6), and ectopic lipid storage.20, 21
In the present study, although the liver enzymes alanine aminotransferase and γ-glutamyl transferase, biomarkers of nonalcoholic fatty liver and the related metabolic syndrome,22, 23 were not independent correlates of central obesity normal weight status in the multivariate analysis, the levels of these enzymes were significantly greater in the central obesity normal weight group, after controlling for age, race, and gender. It has been suggested that central obesity normal weight persons tend to accumulate fat in nonphysiologic depots such as the liver and muscle.24 In the present study, plasma uric acid was also significantly greater in the central obesity normal weight group. That central obesity and related insulin resistance are risk factors for hyperuricemia and gout is well known.25
This community-based study had certain limitation in that it lacked a direct assessment of the body fat mass and distribution, ectopic liver fat content, and in vivo insulin action. We used well-established simple surrogate measures. Furthermore, the present study was observational and cross-sectional in nature and, therefore, could not address the issue of causality, but only suggest putative mechanisms for the observed relations. In conclusion, the results of the present study have underscored the utility of the waist-to-height ratio in detecting asymptomatic normal weight younger adults with central obesity and related adverse cardiometabolic risk factors and their burden on subclinical atherosclerosis. These observations have implications for preventive cardiology.
Acknowledgment
The Bogalusa Heart Study was a joint effort of many investigators and staff members whose contributions are gratefully acknowledged. We especially thank the study participants.
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This study was supported by Grant AG-16592 from the National Institute on Aging, Bethesda, Maryland, and Grants 0855082E and 0555168B from the American Heart Association, Dallas, Texas.
PII: S0002-9149(09)01005-4
doi:10.1016/j.amjcard.2009.04.037
© 2009 Elsevier Inc. All rights reserved.
