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      The "lipid accumulation product" performs better than the body mass index for recognizing cardiovascular risk: a population-based comparison

      research-article
      1 ,
      BMC Cardiovascular Disorders
      BioMed Central

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          Abstract

          Background

          Body mass index (BMI, kg/m 2) may not be the best marker for estimating the risk of obesity-related disease. Consistent with physiologic observations, an alternative index uses waist circumference (WC) and fasting triglycerides (TG) concentration to describe lipid overaccumulation.

          Methods

          The WC (estimated population minimum 65 cm for men and 58 cm for women) and TG concentration from the third National Health and Nutrition Examination Survey (N = 9,180, statistically weighted to represent 100.05 million US adults) were used to compute a "lipid accumulation product" [LAP = (WC-65) × TG for men and (WC-58) × TG for women] and to describe the population distribution of LAP. LAP and BMI were compared as categorical variables and as log-transformed continuous variables for their ability to identify adverse levels of 11 cardiovascular risk factors.

          Results

          Nearly half of the represented population was discordant for their quartile assignments to LAP and BMI. When 23.54 million with ordinal LAP quartile > BMI quartile were compared with 25.36 million with ordinal BMI quartile > LAP quartile (regression models adjusted for race-ethnicity and sex) the former had more adverse risk levels than the latter (p < 0.002) for seven lipid variables, uric acid concentration, heart rate, systolic and diastolic blood pressure. Further adjustment for age did not materially alter these comparisons except for blood pressures (p > 0.1). As continuous variables, LAP provided a consistently more adverse beta coefficient (slope) than BMI for nine cardiovascular risk variables (p < 0.01), but not for blood pressures (p > 0.2).

          Conclusion

          LAP (describing lipid overaccumulation) performed better than BMI (describing weight overaccumulation) for identifying US adults at cardiovascular risk. Compared to BMI, LAP might better predict the incidence of cardiovascular disease, but this hypothesis needs prospective testing.

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          Most cited references35

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          Waist circumference and not body mass index explains obesity-related health risk.

          The addition of waist circumference (WC) to body mass index (BMI; in kg/m(2)) predicts a greater variance in health risk than does BMI alone; however, whether the reverse is true is not known. We evaluated whether BMI adds to the predictive power of WC in assessing obesity-related comorbidity. Subjects were 14 924 adult participants in the third National Health and Nutrition Examination Survey, grouped into categories of BMI and WC in accordance with the National Institutes of Health cutoffs. Odds ratios for hypertension, dyslipidemia, and the metabolic syndrome were compared for overweight and class I obese BMI categories and the normal-weight category before and after adjustment for WC. BMI and WC were also included in the same regression model as continuous variables for prediction of the metabolic disorders. With few exceptions, overweight and obese subjects were more likely to have hypertension, dyslipidemia, and the metabolic syndrome than were normal-weight subjects. After adjustment for WC category (normal or high), the odds of comorbidity, although attenuated, remained higher in overweight and obese subjects than in normal-weight subjects. However, after adjustment for WC as a continuous variable, the likelihood of hypertension, dyslipidemia, and the metabolic syndrome was similar in all groups. When WC and BMI were used as continuous variables in the same regression model, WC alone was a significant predictor of comorbidity. WC, and not BMI, explains obesity-related health risk. Thus, for a given WC value, overweight and obese persons and normal-weight persons have comparable health risks. However, when WC is dichotomized as normal or high, BMI remains a significant predictor of health risk.
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            Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome.

            The underlying pathophysiology of the metabolic syndrome is the subject of debate, with both insulin resistance and obesity considered as important factors. We evaluated the differential effects of insulin resistance and central body fat distribution in determining the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III. In addition, we determined which NCEP criteria were associated with insulin resistance and central adiposity. The subjects, 218 healthy men (n = 89) and women (n = 129) with a broad range of age (26-75 years) and BMI (18.4-46.8 kg/m2), underwent quantification of the insulin sensitivity index (Si) and intra-abdominal fat (IAF) and subcutaneous fat (SCF) areas. The metabolic syndrome was present in 34 (15.6%) of subjects who had a lower Si [median: 3.13 vs. 6.09 x 10(-5) min(-1)/(pmol/l)] and higher IAF (166.3 vs. 79.1 cm2) and SCF (285.1 vs. 179.8 cm2) areas compared with subjects without the syndrome (P < 0.001). Multivariate models including Si, IAF, and SCF demonstrated that each parameter was associated with the syndrome. However, IAF was independently associated with all five of the metabolic syndrome criteria. In multivariable models containing the criteria as covariates, waist circumference and triglyceride levels were independently associated with Si and IAF and SCF areas (P < 0.001). Although insulin resistance and central body fat are both associated with the metabolic syndrome, IAF is independently associated with all of the criteria, suggesting that it may have a pathophysiological role. Of the NCEP criteria, waist circumference and triglycerides may best identify insulin resistance and visceral adiposity in individuals with a fasting plasma glucose <6.4 mmol/l.
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              Adipose tissue as a buffer for daily lipid flux.

              K. Frayn (2002)
              Insulin resistance occurs in obesity and Type II (non-insulin-dependent) diabetes mellitus, but it is also a prominent feature of lipodystrophy. Adipose tissue could play a crucial part in buffering the flux of fatty acids in the circulation in the postprandial period, analogous to the roles of the liver and skeletal muscle in buffering postprandial glucose fluxes. Adipose tissue provides its buffering action by suppressing the release of non-esterified fatty acids into the circulation and by increasing triacylglycerol clearance. In particular, the pathway of 'fatty acid trapping' (adipocyte uptake of fatty acids liberated from plasma triacylglycerol by lipoprotein lipase) could play a key part in the buffering process. If this buffering action is impaired, then extra-adipose tissues are exposed to excessive fluxes of lipid fuels and could accumulate these in the form of triacylglycerol, leading to insulin resistance. These tissues will include liver, skeletal muscle and the pancreatic beta cell, where the long term effect is to impair insulin secretion. Adipose tissue buffering of lipid fluxes is impaired in obesity through defects in the ability of adipose tissue to respond rapidly to the dynamic situation that occurs after meals. It is also impaired in lipodystrophy because there is not sufficient adipose tissue to provide the necessary buffering capacity. Thus, the phenotype, at least with regard to insulin resistance, is similar with both excess and deficiency of adipose tissue. Furthermore, this concept could provide a framework for understanding the action of the thiazolidinedione insulin-sensitizing agents.
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                Author and article information

                Journal
                BMC Cardiovasc Disord
                BMC Cardiovascular Disorders
                BioMed Central (London )
                1471-2261
                2005
                8 September 2005
                : 5
                : 26
                Affiliations
                [1 ]National Center for Chronic Disease Prevention and Health Promotion, CDC, Mail-stop K-10, 4770 Buford Highway, Atlanta, Georgia 30341-3717 USA
                Article
                1471-2261-5-26
                10.1186/1471-2261-5-26
                1236917
                16150143
                aabd6987-4d73-4e9a-8a28-f6ffb943509d
                Copyright © 2005 Kahn; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 2 March 2005
                : 8 September 2005
                Categories
                Research Article

                Cardiovascular Medicine
                Cardiovascular Medicine

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