Use of waist circumference to predict insulin resistance: retrospective study
BMJ 2005; 330 doi: https://doi.org/10.1136/bmj.38429.473310.AE (Published 09 June 2005) Cite this as: BMJ 2005;330:1363
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Abdominal obesity, as measured by waist circumference, is a key predictive measurement of metabolic and cardiovascular risk, more accurate than the measurement of Body Mass Index (BMI) alone.1
While there is some debate over the exact threshold, the principle is clear – a measurement of over 100cm/ 40 inches is regarded as significantly increasing risk in men. We believe it is vital that waist circumference be used as a standard test to ensure the accurate assessment of patients at high risk of metabolic and cardiovascular disease (CVD) and that waist circumference should be given the same importance as a routine blood pressure or cholesterol checks.
Abdominal obesity is a measure of excess visceral fat. Visceral fat, the accumulation of adipose tissue within the omentum, abdomen and around abdominal organs can be assessed simply by measuring waist circumference. It is a key factor in the development and progression of cardiovascular disease. It is believed that the close proximity of visceral fat to the hepatic portal circulation, and the cytokines (including tumour necrosis factor-á, interleukin-6 and C-reactive proteins) secreted by the adipocytes directly influence risk factors associated with the development of cardiovascular disease.2 Waist circumference is therefore an effective and simple tool which could be integrated into general practice.
Weight reduction in obese patients at risk of CVD is associated with an improvement in metabolic factors and improved glycaemic control.3 A modest reduction in weight of approximately 5–10% has been shown to lead to significant reductions in blood pressure, thrombogenic potential and inflammatory markers, as well as improvements in lipid profile and insulin sensitivity.4 Recent studies support the benefits of reducing waist circumference to improve metabolic parameters and cardiovascular risk.5,6
There is therefore an urgent need to include the measurement of waist circumference in the current review of GMSII. Its inclusion would enable both easier identification of high-risk patients and earlier implementation of management strategies.
Kind regards
Dr David Haslam GP and Chairman of the National Obesity Forum
Dr Henry Purcell Senior Fellow in Cardiology, Royal Brompton Hospital, London.
Dr Nick Finer Senior Research Associate, University of Cambridge School of Clinical Medicine and Hon Consultant in Obesity Medicine, Addenbrooke's Hospital Cambridge
Dr John Reckless Consultant, Endocrinologist Royal United Hospital Bath, & Honorary Reader in Medicine, University of Bath
Prof Anthony Barnett Professor of Medicine at the University of Birmingham and Consultant Physician at Central England NHS Foundation Trust (formerly Birmingham Heartlands and Solihull NHS Trust (Teaching))
Dr Howard Stoate, GP & MP
Louise Diss Managing Director, The Obesity Awareness & Solutions Trust
References: 1. Yusuf S, et al; Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study), The Lancet, September 2004 2. Perry C, et al, Adipose tissue: passive sump or active pump? Br J Diabetes Vasc Dis 2001;1:110-4 3. Quality and outcomes framework guidance. Published May 2003 (updated August 2004). The British Medical Association. http://www.bma.org.uk/ap.nsf/Content/QualityOutcomes 4. Sharma AM. Adipose tissue: a mediator of cardiovascular risk. International Journal of Obesity (2002); 26: Suppl 4, S5-S7 5. Van Gaal, L. RIO-Europe. Lancet. 2005; tbc 6. Wang, Y et al. Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men. Am J Clin Nutr. 2005; 81:555-63
Competing interests: None declared
Competing interests: No competing interests
The authors are to be highly complimented for their clear, concise paper presentation of the "Use of waist circumference to predict insulin resistance:Retrospective study".(1)
Waist circumference as indicated by the authors <100 CM for both sexes becomes a clinical quideline that excludes insulin resistance in patients under investigation for biochemical abnormality in pre and established type 2 diabetic patients or the obese dysmetabolic syndrome.
This paper suggests new and reasonable approaches to treating obese patients with abnormal protuberant abdomens, with waist circumference exceeding 100 CM. towards preventing the establishment of insulin resistance, however, requiring evidence based clinical studies. These approaches are: 1- How effective are abdominal exercises for protuberant abdomens with waist circumference of 100 CM or more, in reducing or excluding the development of insulin resistance? and 2-The same question for liposuction ?
Liposuction has its own operative risks and may not be suitable for all patients and its risks have to be weighed carefully against its benefits.
Reference: (1) BMJ 2005;0;bmj.38429.473310.AEv1
Competing interests: None declared
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I agree with Wahrenberg et al, that Body Mass Index alone is not the best predictor of insulin resistance or as a main parameter to estimate the cardiovascular risk or the metabolic syndrome. His findings on waist circumference can be a good guide, but could also be insufficient.
I have been testing for years the Pulse by Mass Index (PMI), which combines Body Mass Index (BMI) with the Resting Heart Rate (RHR), basal, fasting, early in the morning, or more than two hours after a mealtime.
PMI is equal to BMI by RHR divided by 1730 (24x72): BMIxRHR/1730.
I have confirmed over the years, after our first preliminary report in Lancet 1999 (1), that the PMI correlates very highly with the global cardiovascular risk calculated with the Framingham risk equation. For instance, a 45 years old man with a BMI of 30 and a RHR of 60 has less global risk than the same man with a RHR of 90 (PMI of 1.04 vs. PMI of 1.56, which would probably correlate with a global risk of less than 10 % vs. more than 20 to 30 %).
Overweight is a first range risk factor, and every unit in excess of BMI implies an excess in mortality due to cardiovascular disease of about 8 to 10 %. Moreover, caloric restriction has consistently increased the lifespan in all species studied.
The importance of resting heart rate as a cardiovascular risk factor has been increasingly recognized since the studies of Framingham and Göteborg, reinforced by the success of Betablockers in coronary heart disease, congestive heart failure and perioperative mortality in high risk patients. Recently, heart rate variability, chronotropic incompetence and heart rate recovery after exercise, have demonstrated to be predictors of mortality. In all mammals, the slower the pulse, the longer the lifespan, and viceversa. Physical fitness and the regular practice of exercise usually reduce the RHR and improve the PMI and the cardiovascular risk.
The Pulse×Mass Index reflects overweight, stress, sympathetic stimulation, oxidative metabolic rate, hyperinsulinemia, inflammatory activity, physical fitness and side effects of drugs like water retention, potent vasodilation and tachycardia. The therapeutic interventions, like diet, exercise or drugs, should improve the treated cardiovascular risk factor without increasing, or better reducing the Pulse×Mass Index.
Thus, pulse×mass index, a widely accessible index of physical signs, appears to be predictive of the cardiovascular risk, and can contribute together with waist circumference and the known risk factors, to a more complete assessment of cardiovascular risk. It should be done routinely in every patient.
Reference. Sánchez-Delgado E and Liechti H. Lifetime risk of developing coronary heart disease. Lancet 1999;353:924-925(13 March).
Competing interests: None declared
Competing interests: No competing interests
The common factor here is excessive testosterone, that is, an excessive testosteorne to DHEA ratio. When this occurs, the availability of DHEA is reduced which is connected to this obesity and insulin resistance.
Competing interests: None declared
Competing interests: No competing interests
I was interested to read your article on insulin resistance and the exclusion of risk if waist measurements were <100cm. This seems to be a dangerous statement in light of the results published with the paper and my own experience with insulin resistance, type 2 diabetes and waist measurements less than 100cm.
It is important to remember that obesity is not the only reason for insulin resistance to occur, and may in fact be a secondary effect of insulin resistance itself. There are also a significant number of people with the condition who are genetically pre-disposed to developing insulin resistance without being obese according to the BMI scale.
I find it irresponsible and misleading to make such a statement as was made in this paper and am disappointed in the standard of scientific reporting. If the intention was to say that in the absence of other indicators waist circumference is a good negative indicator then more care needs to be exercised when writing the article. This is especially important as the popular press is now reporting that waist measurements of <100cm do not mean any risk of insulin resistance, which may be leading people to believe they are not at risk when in fact they may be.
Competing interests: None declared
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But the meter is not a good tool for measuring inflammation
Insulin resistance has its anatomic correlate in visceral fat deposition (1).
Imaging studies (e.g. by computed tomography) have proved better accuracy in measuring visceral adipose tissue (VAT) extension and in predicting its metabolic complications (2). Even so these techniques are not properly feasible for clinical use.
It is in this sense that the present study (3) is a warning for future clinical approach to the obese patient. Reducing waist cut-off values seems to be of real benefit in a more and more preventive medicine, and this particularly to the lights of recent discoveries. Inflammatory background, through adipose tissue macrophage infiltration, has been demonstrated to increase proportionally to adiposity (4)and VAT has been fingered as an important source of imflammatory molecules such monocyte chemoattractant protein 1 (MCP-1) (5).
Just because a lower waist circumference suggests protection from insulin resistance (3), it doesn’t mean a low-inflammatory-syndrome, with possible detrimental effects on cardiac morpho-function, may not exist (5).
It is noteworthy that inflammatory activation within adipose tissue has been suggested to occur before the onset of insulin resistance, indicating itself as a sort of precondition (4). In our previous issue we reported that severely obese women (BMI > 40 Kg/m2) with grater amount of visceral fat deposition (VAT area > 130 cm2 vs VAT area < 130 cm2 as measured by computed tomography) presented higher values of MCP-1 (5). Same results in this group have been observed also for many other inflammatory markers linked to visceral adiposity such as C-reactive protein, interleukine-6, soluble interleukine -6 receptor (sIL-6R), TNF-alpha, soluble TNF-alpha receptor I (sTNFRI), fibrinogen and VES even in presence of normal glucose tolerance (HOMA: 2.8±1.3) (unpublished data).
Thus if a waist < 100 cm seems to exclude insulin resistance by the other hand the same can not be sustained for silent inflammation and additional studies should be performed with this regard.
Why don’t finding a meter also for this?
References:
1. Montague CT, O'Rahilly S. The perils of portliness: causes and consequences of visceral adiposity. Diabetes. 2000 Jun;49(6):883-8
2. Nicklas BJ, Penninx BW, Ryan AS, Berman DM, Lynch NA, Dennis KE. Visceral adipose tissue cutoffs associated with metabolic risk factors for coronary heart disease in women. Diabetes Care. 2003 May;26(5):1413-20
3. Wahrenberg H, Hertel K, Leijonhufvud BM, Persson LG, Toft E, Arner P. Use of waist circumference to predict insulin resistance: retrospective study. BMJ. 2005 Jun 11;330(7504):1363-4
4. Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, Sole J, Nichols A, Ross JS, Tartaglia LA, Chen H. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003 Dec;112(12):1821-30
5. Malavazos AE, Cereda E, Morricone L, Corsi MM, Ambrosi B. Monocyte chemoattractant protein-1 in adipose tissue. J Clin Endocrinol Metab. 2005 May;90(5):3128
Competing interests: None declared
Competing interests: No competing interests