Education Resource from the Society for Endocrinology

Metabolic Syndrome: screening and prevention

Dr Simon Griffin

Strangeways Research Laboratory, Cambridge

Summer School 11-14 July 2006
The Møller Centre, Storeys Way, Cambridge, UK

Screening is ‘the systematic application of a test or inquiry, to identify individuals at sufficient risk of a specific disorder to warrant further investigation or direct preventive action, amongst persons who have not sought medical attention on account of symptoms of that disorder¹. Given this ethical difference between screening and routine medical practice specific criteria need to be met before population screening can be recommended.2 While the metabolic syndrome (MS) might be regarded as an important health problem its epidemiology and natural history are insufficiently understood. There is disagreement over the choice of a simple, safe, precise, valid, acceptable test with agreed cut-offs. There is no definitive evidence that earlier detection and treatment of MS is associated with improved outcomes and outweighs any associated harms. In particular, there is no trial evidence of cost-effectiveness of a screening programme for MS, although this is also true of established programmes such as cervical screening.

The various definitions of MS comprise somewhat arbitrary cut-offs for a range of continuously distributed risk factors for the development of type 2 diabetes and coronary heart disease. Depending on the choice of definition the label could be applied to around a third of the adult population in this country. It is not clear whether attribution of such a label, and hence ‘medicalising’ increasing proportions of society, is associated with beneficial changes in relevant health behaviours (in particular diet and physical activity), increased therapeutic interventions (advice and drug treatment) from health professionals, or excessive anxiety, increased absenteeism from work and reductions in self-rated health. Furthermore, given that the majority of those screened will be negative there is concern about the extent of false reassurance, that is to say those with results below a given threshold adopting less healthy behaviours and consequently increasing both their own and the overall population risk. Such outcomes have been reported following screening for a range of different cardiovascular risk factors such as blood pressure and cholesterol³

MS and related abnormalities and complications result from interactions between genetic and environmental (in particular behavioural) determinants. Preventive strategies can target individuals and sub-groups at increased risk or, as Geoffrey Rose demonstrated in the case of cholesterol, aim to shift the whole population distribution for given risk factors⁴. Modelling studies suggest that a range of different approaches to the prevention of diabetes, from surgery for the severely obese through to mass media campaigns promoting healthy lifestyles, are likely to be cost-effective ⁵. At present the strongest evidence for diabetes prevention comes from trials of intensive behavioural interventions and the use of drugs such as hypoglycaemic agents among individuals with impaired glucose tolerance (IGT)⁶. However, there are easier ways of identifying those at increased risk of developing diabetes than population screening for MS or IGT, for example through the use of questionnaires or risk scores based on data routinely collected in primary care ⁷. It also appears that relatively small changes in diet and physical activity at the population level might have a greater impact on overall diabetes incidence than targeting those with IGT or MS ⁸. Furthermore, given that there is no evidence that treatment of MS is more effective than treatment of its individual components it remains to be seen whether characterising individuals according to their MS status will contribute significantly to preventive strategies.

1. National Screening Committee, Department of Health, 1998.
2. Wilson JGM, Jungner G. Geneva: WHO, 1968.
3. Tymstra T, Bieleman B. Fam Pract 1987;4:287-290.
4. Rose G. BMJ 1981;282:1847-1851.
5. Segal L et al. Health Promotion International 1998;13:197-209.
6. The DPP Research Group. NEJM 2002;346:393-403.
7. Griffin SJ, Little PS, Hales CN, Kinmonth AL, Wareham NJ. Diabetes/Metab Res Rev 2000;16:164-171.
8. Simmons RK, Harding A-H, Jakes RW, Wareham NJ, Griffin SJ. Diabetologia 2006;49:905-911.

The opinions expressed in this paper are those of the speaker and do not necessarily reflect the views of the Society

Revised: 23-Aug-2006