Unit for Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, PO Box 609, SE-751 25 Uppsala, Sweden

Correspondence to: M Öhrvall, Unit for Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, PO Box 609, SE-751 25 Uppsala, Sweden. Margareta.Ohrvall@geriatrik.uu.se

BACKGROUND: Abdominal adiposity has been described as an independent risk factor for coronary heart disease. Sagittal abdominal diameter has been found to be closely related to the amount of visceral adipose tissue.

AIM: To compare the sagittal abdominal diameter with other anthropometric measures regarding their relationships to risk factors for coronary heart disease (CHD).

DESIGN: A study of 885 men and women participating in a health survey.

MEASUREMENTS: Sagittal abdominal diameter, body mass index (BMI), waist and hip circumferences, waist-to-hip ratio, serum concentrations of risk factors for CHD, blood pressure.

RESULTS: In men the sagittal abdominal diameter showed stronger correlations to the CHD risk factors serum cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, glucose, insulin, apolipoprotein B (apoB), plasminogen activator inhibitor tissue-type plasminogen activator (t-PA) and lipid-corrected alpha tocopherol, and to systolic and diastolic blood pressures than the other anthropometric measurements. In women, compared with the other anthropometric measurements the sagittal abdominal diameter was more strongly correlated to serum cholesterol, LDL cholesterol, LDL/HDL (high-density lipoprotein), apo B and t-PA, and to systolic and diastolic blood pressure. The sagittal abdominal diameter showed a stronger correlation to 'total risk' for cardiovascular disease (+0.66 for men, +0.62 for women), than waist circumference (+0.63 for men, +0.57 for women) and waist-to-hip ratio (+0.61 for men and +0.48 for women; P<0.0001 for all correlations). This diameter was also more strongly correlated to 'metabolic risk' (+0.64 for men, +0.59 for women) than waist circumference (+0.60 for men, +0.59 for women) and waist-to-hip ratio (+0.58 for men, +0.52 for women)(P<0.0001 for all correlations). In a regression analysis including the anthropometric measurements and the risk values, the sagittal diameter was the strongest measure of cardiovascular risk in both men and women.

CONCLUSIONS: Among both men and women in this study the sagittal abdominal diameter showed stronger correlations to cardiovascular risk and to other risk factors in the metabolic syndrome than other anthropometric variables such as waist circumference, waist-to hip ratio and BMI.

International Journal of Obesity (2000)24, 497-501

sagittal abdominal diameter; anthropometric measurement; cardiovascular risk

Introduction

Atherosclerotic cardiovascular diseases are the major causes of morbidity and mortality in the Western world. Among established risk factors for coronary heart disease (CHD) connected with the metabolic syndrome are elevated concentrations of serum triglycerides, low concentrations of high density lipoprotein (HDL) cholesterol, hyperinsulinaemia, type 2 diabetes, hypertension and high concentrations of plasminogen activator inhibitor (PAI-1). Abdominal adiposity has been described as an independent risk factor for CHD¹ and the abdominal fat distribution as reflected by the waist-to-hip ratio is a stronger predictor for CHD than body weight.² Among other anthropometric measurements the sagittal abdominal diameter (SAD) has been reported to be most closely related to the amount of visceral adipose tissue.³ The aim of this study was to measure this diameter and to compare it with other anthropometric measures reflecting the metabolic syndrome with regard to their relationship to risk factors for CHD in men and women participating in a health survey.

Subjects

A health survey concerning risk factors for coronary heart disease was carried out among the employees of a Swedish telephone company in Uppsala, Sweden. Nine hundred and six (90%) of the employees participated, about half of whom were blue-collar and about half white-collar workers. Twelve subjects were excluded because of concurrent diseases: one with untreated hypothyroidism, three with insulin-dependent diabetes mellitus, three with treated malignant disease, one who had undergone a kidney transplantation and four who were being treated with cortisone. Nine further women were excluded because of pregnancy.

The mean age of the remaining 885 participants (588 males and 297 females) was 41.0 y (19-66 y) and their median age was 41.5 y. Four subjects had non-insulin-dependent diabetes mellitus, 15 used contraceptive pills and 13 were receiving postmenopausal hormone replacement therapy. Twenty-eight were being treated with beta-blockers and diuretics and two with diuretics only. Seven were having replacement therapy for hypothyroidism¾they were all euthyroid at the time of the survey.

Methods

Blood samples were drawn after a 12 h overnight fast. Neither smoking nor heavy physical activity were allowed in the morning before the examination. Blood sampling and all measurements, including anthropometric measurements and blood pressure, were performed by the same observer. Supine blood pressure was measured after 10 min rest (mean of two values obtained at a 2 min interval). The waist and hip circumferences were measured with the subject in the supine position. SAD was recorded at the umbilical level as the height of the abdomen measured from the examination couch when lying down with the legs straight. The body mass index (BMI) was calculated as body weight (in kilograms) divided by height (in metres) squared.

Lipoprotein lipid concentrations in serum were determined. Very low density lipoprotein (VLDL), low density lipoprotein (LDL) and HDL were isolated by a combination of preparative ultracentrifugation⁴ and precipitation with a sodium phosphotungstate and magnesium chloride solution.⁵ Triglyceride and cholesterol concentrations were measured in serum and in the isolated lipoprotein fractions by enzymatic methods, using IL Test Cholesterol Trinder's Method 181618-80 and IL Test Enzymatic-colorimetric Method 181709-00 in a Monarch apparatus (Instrumentation Laboratories, Lexington, MA, USA).

Plasma glucose was assayed by the glucose oxidase method.⁶ Serum insulin was measured by the Phadebas Insulin Test (Pharmacia, Uppsala, Sweden).⁷ PAI-1 activity in plasma was measured with Spectolyse/ pL kits from Biopool AB (Umeå, Sweden), using polylysine as a stimulator.⁸ For measurement of the plasma concentration of tissue-type plasminogen activator (t-PA) antigen, Imolyse % t-PA antigen kits (Biopool AB) were used.⁹ The serum concentrations of apolipoprotein A-1 (apo A-1) and B (apo B) were determined by immunoturbidimetry in a Monarch apparatus.

Serum alpha tocopherol concentrations were assayed by HPLC, using a fluorescence detector as described earlier.¹⁰ The serum tocopherol levels are reported as the concentration corrected for the sum of serum cholesterol and serum triglycerides as suggested by Thumhamn et al.¹¹

Statistical methods

Descriptive statistics given are number of observations, mean, standard deviation and range. A 'metabolic risk' score (reflecting metabolic aberrations related to the metabolic syndrome) was calculated, and comprised serum triglycerides, HDL cholesterol, fasting glucose, fasting insulin and PAI-1, and supine systolic and diastolic blood pressures. A 'total risk' score was also calculated, comprising the items included in the metabolic risk score plus serum cholesterol, LDL cholesterol, LDL/HDL ratio, t-PA, apo B, apo A-1 and lipid-corrected alpha tocopherol. Each item was converted to quintiles. For all items except HDL cholesterol and alpha tocopherol the 20% lowest values were given the quintile value 1 and so on. HDL cholesterol and alpha tocopherol were given quintile numbers in the reverse order, so that the 20% subjects with the lowest values were given the quintile value 5 etc. The risk score was calculated as the sum of quintiles over all items. The relation between the metabolic risk score and each of the four anthropometric variables was analysed using the Spearman correlation coefficient. Differences between the SAD correlations to the risk scores and the other anthropometric variables correlation to risk scores were tested for statistical significance using the method described by Morrison.¹²

To evaluate the relative importance of the anthropometric variables, a multiple stepwise linear regression model on metabolic score, using the four anthropometric variables as candidate predictors, was estimated. All analyses were performed for all subjects and separately for men and women.

Results

The mean SAD was 23.5 (17.0-34.5) cm in men and 21.7 (15.5-32.0) cm in women. The mean waist-to-hip ratio was 0.90 (0.76-1.13) in men and 0.81 (0.64-1.06) in women and the mean waist circumference was 88.2 (71.0-128.0) cm in men and 78.9 (62.0-115.0) cm in women. Men had a mean BMI of 24.9 (17.4-39.7) kg/m² and women 23.8 (16.2-40.8) kg/m² (Table 1). The lipid, glucose, insulin, PAI-1 and lipid-corrected alpha tocopherol concentrations in serum and the mean systolic and diastolic pressures are presented in Table 2.

In men, compared with the other anthropometric measurements SAD was more strongly correlated to the serum concentrations of cholesterol, LDL cholesterol, serum triglycerides, glucose, insulin, apo B, PAI-1, t-PA and lipid-corrected alpha tocopherol, and to the systolic and diastolic blood pressures (Table 3). In women SAD showed stronger correlations to serum cholesterol, LDL cholesterol, LDL/HDL, apo B and t-PA and to systolic and diastolic blood pressures compared with the other anthropometric variables (Table 4). There was no significant difference in the correlation between SAD and risk variables with increasing obesity, when tested in subjects with BMI below and above 26 kg/m².

SAD was more closely correlated to 'total risk' (+0.66, P<0.0001 for men, +0.62, P<0.0001 for women), than waist circumference (+0.63, P<0.0001 for men and +0.57, P<0.0001 for women) and waist-to-hip ratio (+0.61, P<0.0001 for men and +0.48, P<0.0001 for women). SAD was also more strongly correlated to 'metabolic risk' (+0.64, P=0.0001 for men, +0.59, P=0.0001 for women) than waist circumference (+0.60, P<0.0001 for men and +0.59, P<0.0001 for women) and waist-to-hip ratio (+0.58, P<0.0001 for men and +0.52, P<0.0001 for women; Table 5). SAD was in all subjects significantly more closely correlated (P<0.01) to 'total risk' and 'metabolic risk' than waist, waist-to-hip ratio and BMI were to these risk parameters. When the correlations between the anthropometric measurements and the cardiovascular risk factors were adjusted for age, the correlation were slightly weaker but in the same ranking order as without adjustment, except for older women where waist was more strongly correlated to risk factors than SAD. In a regression analysis including the anthropometric measurements and the risk values the SAD showed the strongest association with risk in both men and women. 40% of the variation in risk could be explained by SAD and only 4% could be further explained by the other three anthropometric variables. When SAD, waist circumference and the waist-to-hip ratio were corrected for height, the correlations to some of the risk parameters became slightly stronger than without correction. The strongest associations, however, were still noted for height-corrected SAD compared with height-corrected waist circumference and waist-to-hip ratio (Table 6).

Discussion

Waist circumference has been claimed to be a strong marker for health risk, since the abdominal fat distribution is associated with risk factors for CHD ¹³ and diabetes type 2.¹⁴ It has also been shown in a large study that people with a large waist circumference suffer impairment of both health and quality of life.¹⁵

Among both men and women in this study, SAD was found to have stronger correlations to the risk factors in the metabolic syndrome than the other measured anthropometric variables, namely waist circumference, waist-to-hip ratio and BMI. In the regression analysis the most important marker for risk factors for CHD and for the metabolic syndrome was SAD.

Pouliot et al have shown that waist circumference and SAD are the best simple anthropometric indices of abdominal and visceral adipose tissue accumulation and of cardiovascular risk in men and women.¹⁶ The mechanism of the proposed link between increased visceral adipose tissue and risk factors for CHD may be the occurrence of elevated concentrations of free fatty acids in blood from the enlarged abdominal fat depots. By a multiscan CT technique the SAD at the umbilical level has been shown to predict the amount of visceral adipose tissue.³

In recent studies^16,17 SAD has been measured on CT scans, but in our study it was measured with the patient in a supine position using a simple ruler. We have shown that measurement of SAD by this easy method is reproducible and accurate and can be used to estimate the cardiovascular risk situation in these patients (unpublished).

In a study by Richelsen and Pedersen,¹⁸ 58 men participated in a study in which SAD was measured with a calliper. Besides SAD, the ratio between SAD and height showed a strong association with risk factors in that study. It has also been reported that the ratio of SAD to height is a strong indicator of coronary risk as measured by the Framingham risk index.¹⁹ In our study SAD corrected for height showed a slightly stronger association with some of the risk factors than uncorrected SAD. However, the height-corrected SAD was still more strongly correlated to risk than were the height-corrected waist circumference and waist-to-hip ratio. It has been pointed out that the ratio of waist circumference to height may be more strongly correlated to risk factors for coronary heart disease than waist circumference per se, and that the reason for using height is that it can take into account the fact that women may be shorter than men at the same degree of risk.^20,21

SAD is usually studied in relatively small populations, usually of only men. In our study we have confirmed that a high SAD is an important risk parameter in a large reference population including both men and women. We have also shown that risk factors for coronary heart disease such as PAI-1 and t-PA are positively correlated to SAD. The lipid-corrected concentration of alpha tocopherol was negatively correlated to SAD, as observed before in this population.¹⁰ The relations between these parameters and SAD do not appear to have been studied previously.

1 Larsson B, Svärdsudd K, Welin L, Wilhelmsen L, Björntorp P, Tibblin G. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in 1913. Br Med J 1984; 288: 1401-1404.

2 Lapidus L, Bengtsson C, Larsson B, Pennert K, Rybo E, Sjöström L. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow up of participants in the population study of women in Gothenburg, Sweden. Br Med J 1984; 289: 1257-1261.

3 Kvist H, Chowdhury B, Grangård U, Tylén U, Sjöström L. Total and visceral adipose-tissue volumes derived from measurements with computed tomography in adult men and women: predicted equations. Am J Clin Nutr 1988; 48: 1351-1361. MEDLINE

4 Havel RJ, Eder HA, Bragdon JH. The determination and chemical composition of ultracentrifugally separated lipoproteins in human serum. J Clin Invest 1955; 34: 1345-1353.

5 Seigler L, Wu WT. Separation of serum high-density lipoprotein for cholesterol determination: ultracentrifugation vs precipitation with sodium phosphotungstate and magnesium chloride. Clin Chem 1981; 27: 838-841. MEDLINE

6 Hjelm M, deVerdier CH. A methodological study of the enzymatic determination of glucose in blood. Scand Clin Lab Invest 1963; 15: 415-428.

7 Wide L, Axen R, Porath J. Radioimmunosorbent assay of proteins, chemical couplings of antibodies to insoluble dextran. Immunochemistry 1967; 4: 381.

8 Eriksson E, Rånby M, Gyzander E, Risberg B. Determination of plasminogen activator inhibitor in plasma using t-PA and a chromogenic single point poly-D-lysine stimulated assay. Thromb. Res. 1988; 50: 90-101.

9 Rånby M, Bergsdorf N, Nilsson T, Mellbring G, Winblad B, Bucht G. Age dependence of tissue plasminogen activator concentrations in plasma, as studied by an improved enzyme-linked immunosorbent assay. Clin chem 1986; 32: 2160-2165. MEDLINE

10 Öhrvall M, Tengblad S, Vessby B. Lower tocopherol serum levels in subjects with abdominal adiposity. J Intern Med 1993; 234: 53-60. MEDLINE

11 Thurnhamn DI, Davies JA, Crump BJ, Situnayake RD, Davis M. The use of different lipids to express serum tocopherol: lipid ratios for the measurement of vitamin E status. Ann Clin Biochem 1986; 23: 514-520. MEDLINE

12 Morrison DF. Multivariate statistical methods. McGraw-Hill: New York, 1976, pp 176-179.

13 Han TS, van Leer EM, Seidell JC, Lean MEJ. Waist circumference action levels in the identification of cardiovascular risk factors: prevalence study in a random sample. Br Med J 1995; 311: 1401-1405.

14 Ohlson LO, Larsson B, Svärdsudd K, Welin L, Eriksson H, Wilhelmsen L, Björntorp P, Tibblin G. The influence of body fat distribution on the incidence of diabetes mellitus. 13.5 years of follow-up of the participants in the study of men born in 1913. Diabetes 1985; 34: 1055-1058. MEDLINE

15 Lean MEJ, Han TS, Seidell JC. Impairment of health and quality of life in people with large waist circumference. Lancet 1998; 351: 853-856. MEDLINE

16 Pouliot MC, Després JP, Lemieux S, Moorjani S, Bouchard C, Tremblay A, Nadeau A, Lupien PJ. Waist circumference and abdominal sagittal diameter: Best simple anthropometric indices of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. Am J Cardiol 1994; 73: 460-468. MEDLINE

17 Després JP, Prud'homme D, Pouliot MC, Tremblay A, Bouchard C. Estimation of deep abdominal adipose-tissue accumulation from simple anthropometric measurements in men. Am J Clin Nutr 1991; 54: 471-477. MEDLINE

18 Richelsen B, Pedersen SB. Associations between different anthropometric measurements of fatness and metabolic risk parameters in non-obese, healthy, middle-aged men. Int J Obes 1995; 19: 169-174.

19 Kumlin L, Dimberg L, Mårin P. Ratio of abdominal sagittal diameter to height is strong indicator of coronary risk (letter). Br Med J 1997; 314: 830.

20 Ashwell M, Lejeune S, McPehrson K. Ratio of waist circumference to height may be better indicator of need for weight management (letter). Br Med J 1996; 312: 377.

21 Ashwell M, Cole TJ, Dixon AK. Ratio of waist circumference to height is strong predictor of intra-abdominal fat (letter). Br Med J 1996; 313: 559-560.

Table 1 Anthropometric measurements

Table 2 Clinical characteristics

Table 3 Correlation coefficients between anthropometric measurements and risk factors for coronary heart disease in men, n=588

Table 4 Correlation coefficients between anthropometric measurements and risk factors for coronary heart disease in women, n=297

Table 5 Correlations* between anthropometric measurements and risk. Men: n=588; women: n=297

Table 6 Correlation coefficients between anthropometric measurements corrected for height and risk factors for coronary heart disease in all subjects