European Heart Journal Advance Access originally published online on October 25, 2007
European Heart Journal 2007 28(23):2954; doi:10.1093/eurheartj/ehm473
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Obesity and its relationship to coronary heart disease: reply
Division of Cardiovascular Diseases Department of Internal Medicine Mayo Clinic College of Medicine Mayo Foundation Rochester, MN USA
Division of Cardiovascular Diseases Department of Internal Medicine Mayo Clinic College of Medicine Mayo Foundation Rochester, MN USA
Division of Cardiovascular Diseases Department of Internal Medicine Mayo Clinic College of Medicine Mayo Foundation Rochester, MN USA
Department of Medicine Atherosclerosis Research Unit Karolinska Institute Sweden
Division of Cardiovascular Diseases Department of Internal Medicine Mayo Clinic College of Medicine Mayo Foundation Gonda 5-368, 200 First Street SW Rochester, MN 55905 USA
Tel: +1 507 284 8087 Fax: +1 507 266 7929 E-mail address: lopez{at}mayo.edu
Das1 raises important points regarding biomarkers produced by adipose tissue, such as free fatty acids (FFAs), cytokines (TNF
and IL-6), and adipokines (leptin and adiponectin) in their relationship to body fat distribution and amount and sex-specific metabolic pathways. Das suggests that measuring these substances might be more relevant to understanding cardiovascular risk at an individual level than measuring adiposity per se.
We agree that adipose tissue deposits in certain regions could be related to greater cardiovascular risk. For example, visceral (primarily omental and mesenteric) rather than total adiposity could have more deleterious effects on the cardiovascular system because of more active adipose tissue in these regions.2 In fact, the association between these biomarkers and visceral/upper-body fat has proved to be stronger when compared with BMI.3,4 However, it may be premature for these biomarkers to replace measurements of body fat for several reasons.
First, although levels of leptin, C-reactive protein, and some cytokines are closely related to body adiposity, it is not yet clear whether these factors are the primary mechanistic pathways of vascular injury on obesity-related atherogenesis. Their effect on the cardiovascular system, independent of degree of body fatness, remains to be determined.5 For example, although lipolysis (in vitro) and subsequent FFA release and elevation of cytokines and adipokines have been shown to be increased in the omental adipose tissue when compared with subcutaneous tissue, subcutaneous fat is known to account for most of the systemic FFA release (
80%).2,5 Moreover, studies have shown that fat cell size itself is related to body fatness and plays a vital role in the production of some of these markers. When compared with small fat cells, large fat cells are metabolically more active and more prone to lipolysis with subsequent release of FFA, cytokines, and adipokines. In fact, after accounting for adipocyte size, the rate of lipolysis is similar in subcutaneous and visceral fat,2 speaking further to the controversy as to how the distribution of fat and the products of fat each account for adverse effects on the cardiovascular system.
Therefore, although these markers may be important to understanding how adipose tissue causes cardiovascular disease, they cannot yet replace the measurement of body fatness (with bioimpedance, air displacement plethysmography, or dual X-ray absorptiometry) or even simple body fat distribution (by waist circumference or waist-to-hip ratio) in the assessment of cardiovascular risk in the clinical context. Furthermore, measurement of these biomarkers is expensive, not widely available, and would require multiple measurements with close longitudinal follow-up, thus limiting their use in clinical practice. In contrast, body composition techniques can be obtained with minimal economic cost and could better stratify patients according to excess in body fatness not identified by BMI alone. Moreover, this interesting concept raised by Das may not be immediately relevant to our data because we studied patients with already established coronary artery disease.
References
- Das UN. Pathophysiology of metabolic syndrome X and its links to the perinatal period. Nutrition (2005) 21:762–773.[CrossRef][Web of Science][Medline]
- Votruba SB, Jensen MD. Regional fat deposition as a factor in FFA metabolism. Annu Rev Nutr (2007) 27:149–163.[CrossRef][Medline]
- Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, Mookadam F, Lopez-Jimenez F. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. Lancet (2006) 368:666–678.[CrossRef][Medline]
- de Koning L, Merchant AT, Pogue J, Anand SS. Waist circumference and waist-to-hip ratio as predictors of cardiovascular events: meta-regression analysis of prospective studies. Eur Heart J (2007) 28:850–856.
[Abstract/Free Full Text] - Jensen MD. Is visceral fat involved in the pathogenesis of the metabolic syndrome? Human model. Obesity (Silver Spring) (2006) 14(Suppl. 1):20S–24S.
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