Understanding cardiometabolic risk

Rising obesity will lead to an increase in cardiovascular disease, advises Professor Mike Kirby

We are seeing increasing numbers of obese patients in our GP practices. In the UK, the proportion of men categorised as obese increased from 13.2 per cent in 1993 to 23.6 per cent in 2004, and for women it rose from 16.4 per cent in 1993 to 23.8 per cent in 2004.

A quarter of the adult population is projected to become obese by 2010. We are therefore going to see a surge in the number of patients with cardiometabolic risk (CMR) factors that might lead to cardiovascular and metabolic diseases in the years to come.

Abdominal obesity

Visceral fat is defined as intra-abdominal fat and is distinct from subcutaneous fat.  Visceral fat has recently been identified as a highly active endocrine organ, not just a storage site for fatty acids.

The adipocytes that make up visceral fat have been shown to secrete many different types of signalling molecules, which have been given the term ‘adipokines’. We are already familiar with several of these – tumour necrosis factor alpha, angiotensinogen and interleukin-6 – others, however, such as adiponectin, have only been discovered recently.

These adipokines play imp-ortant roles in regulating lipid and glucose metabolism, and overall energy homeostatsis.

Based on these observations, we are starting to appreciate the significance of abdominal obesity as a major CMR factor, predisposing individuals to type 2 diabetes and cardiovascular disease (CVD).

In the INTERHEART study, an extensive case-controlled study conducted in over 50 countries, abdominal obes-ity was found to be one of the main modifiable risk factors significantly associated with acute MI. The risks were consistent in all ethnic groups and in men and women worldwide.

Other studies have demonstrated that abdominal obesity is associated with glucose intolerance, insulin resistance and the development of type-2 diabetes; the development of atherogenic dyslipidaemia  and hypertension. The idea of abdominal obesity as a cause of CMR is not new; it was first mooted by the French physician Jean Vague in the 1940s. However, now we have unequivocal evidence.

CMR and its assessment

Abdominally obese patients tend to display numerous abnormalities in their lipid and glucose parameters and can be described as having a high CMR profile. CMR factors are those that lead to CVD and metabolic diseases.

GPs come across these risk factors in patients almost every day. They include insulin resistance, dyslipidaemia (elevated triglycerides, decreased HDL cholesterol ) and hypertension.

Until now, BMI has been used to assess obesity. However, BMI does not differentiate between fat and lean body mass. So, a healthy, muscular athlete with very little adipose tissue may have a BMI of over 27 kg/m2, which would ostensibly classify him as obese. GPs can identify abdominally obese patients with a high CMR profile using a simple measure — waist circumference.

Waist circumference is the simplest measure of visceral fat. It has been suggested that it should be considered a vital sign and recorded in the medical chart of every patient.

The INTERHEART study also identified abdominal obesity as a greater risk factor than BMI, which suggests that measurement of waist circumference would be a better indicator of CMR than BMI.

The International Diabetes Federation has recently developed ethnicity-specific waist circumference cut-off points associated with increased CMR (see box left). These can be used as guidelines for assessment.

According to the UK’s National Obesity Forum, primary care should be at the forefront of managing obesity, as general practice is where most people have first contact with healthcare services.

The Joint British Societies have recommended an opportunistic comprehensive CVD risk assessment for all patients over 40 years of age.

Future strategies

Changes in lifestyle habits, including diet and exercise, are extremely important for the management of CMR, especially abdominal obesity. However, most patients find these lifestyle changes very difficult to maintain in the long term. Therefore, we need to think of additional approaches to adequately support our patients.

One such approach is pharmacotherapy. We have a number of effective therapies that target individual components of CMR, and that can help in improving the lipid profile and glucose metabolism of patients or reduce their BP. 

These include anti-obesity agents such as sibutramine, orlistat and rimonabant; anti-diabetic agents such as insulin and oral therapies such as metformin, glitazones and sulphonylureas; statins for dyslipid-aemias; and anti-hypertensives such as alpha-blockers, ACE-inhibitors and angiotensin ll receptor antagonists.

However, despite the availability of these drugs, a significant number of patients with CMR risk factors do not achieve the clinical targets as defined by current management strategies and the incidences of type-2 diabetes and CVD continue to increase.

Professor Kirby is a GP in Letchworth, Hertfordshire and visiting professor at the University of Hertfordshire

Ethnicity and obesity 

Abdominal obesity and waist circumference thresholds in different ethnic groups

 MenWomen 
European>94 cm (37.0 in) >80 cm (31.5 in)

South Asian

>90 cm (35.4 in)>80 cm (31.5 in)

Chinese

>90 cm (35.4 in)>80 cm (31.5 in)
Japanese>90 cm (35.4 in) >80 cm (31.5 in)

Source: The International Diabetes Federation

References

Health Survey for England 2004 – latest trends. Available at www.ic.nhs.uk/pubs/hlthsvyeng2004upd/2004trendcommentary.pdf/file

National Audit Office. Tackling Obesity in England. 2001. Available at www.nao.org.uk/publications/nao_reports/00-01/0001220.pdf

Carey VJ, Walters EE, Colditz GA, et al . Body fat distribution and risk of non-insulin-dependent diabetes mellitus in women.  Am J Epidemiol. 1997;145: 614–9.

Després JP, Lemieux I, Prud’homme D. Treatment of obesity: need to focus on high risk abdominally obese patients. BMJ 2001; 322: 716–20.

Ding J, Visser M, Kritchevsky SB, et al. The association of regional fat depots with hypertension in older persons of white and African American ethnicity. Am J Hypertens 2004; 17: 971–6.

Harris MM, Stevens J, Thomas N, et al. Associations of fat distribution and obesity with hypertension in a bi-ethnic population: the ARIC study. Obes Res 2000; 8: 516–24.

Nieves DJ, Cnop M, Retzlaff B, et al. The atherogenic lipoprotein profile associated with obesity and insulin resistance is largely attributable to intra-abdominal fat. Diabetes 2003; 52: 172–9. 

Pouliot MC, Despres JP, Nadeau A, et al. Visceral obesity in men. Associations with glucose tolerance, plasma insulin, and lipoprotein levels. Diabetes 1992; 41: 826–34.

Vague J. Sexual differentiation, a factor affecting the forms of obesity. Presse Méd 1947; 30: 339–40.

Wahrenberg H, Hertel K, Leijonhufvud BM, et al. Use of waist circumference to predict resistance: retrospective study. BMJ 2005; 330; 1363–4.

Watanabe J, Tochikubo O. Relationship between visceral fat accumulation and hypertension in obese men. Clin Exp Hypertens 2003; 25: 199–208.

Yusuf S, Hawken S, Ounpuu S et al; Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study). Lancet 2004; 364: 937–52. 

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