WHAT IS TYPE 2 DIABETES MELLITUS?

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CHAPTER 1 WHAT IS TYPE 2 DIABETES MELLITUS?

CLASSIFICATION OF DIABETES MELLITUS

The World Health Organization’s classification of diabetes (WHO 1985) has been adopted internationally. The American Diabetes Association re-examined the diagnostic criteria and classification and recommended modifications in 1997, subsequently agreed by WHO (The Expert Committee 1997, Alberti et al 1998). The terms type 1 and type 2 diabetes (Table 1.1) replaced the old categories of insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The older classification was based upon treatment (many NIDDM patients are on insulin), but did not indicate the nature of the underlying cause (Wroe 1997).

TABLE 1.1 1997–1998 ADA and WHO classification of diabetes mellitus

Type 1
(beta-cell destruction, usually leading to absolute insulin deficiency)
Autoimmune
Idiopathic
Type 2
(may range from predominately insulin resistance with relative insulin deficiency to a predominately secretory defect with or without insulin resistance)
Other specific types
Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas
Endocrinopathies
Drug- or chemical-induced
Infections
Uncommon forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes
Gestational diabetes mellitus (includes gestational impaired glucose tolerance)

Types 1 and 2 diabetes are compared in Table 1.2.

TABLE 1.2 Comparison of the characteristics of types 1 and 2 diabetes mellitus (Beers 1999)

Characteristic Type 1 diabetes Type 2 diabetes
Commonest age at onset Usually <30 years Most often >30 years, but note recent trends
Associated obesity No Yes
Propensity to develop ketoacidosis (requiring insulin to prevent/control) Yes No
Presence of classic symptoms of hyperglycaemia at diagnosis Yes, often severe May be absent
If present, often moderate
Endogenous insulin secretion Very low to undetectable Variable, but low relative to plasma glucose levels
Insulin resistance Not present Yes, but variable
Twin concurrence <50% >90%
Associated with specific HLA-D antigens Yes No
Islet cell antibodies at diagnosis Yes No
Islet pathology Insulitis, selective loss of most beta cells Smaller, normal-looking islets
Amyloid deposits common
Associated increased risks for micro-and macrovascular disease Yes Yes
Hyperglycaemia responds to oral agents No Yes, initially in most patients

© 2006 by Merck & Co., Inc., Whitehouse Station, NJ, USA

CRITERIA AND METHODS FOR THE DIAGNOSIS OF DIABETES MELLITUS

RATIONALE FOR DIAGNOSTIC CRITERIA AND METHODS

The distribution of plasma glucose concentrations is a continuum; so there needs to be a threshold that separates those who are at a substantially increased risk of developing adverse outcomes caused by diabetes from those who are not (The Expert Committee 2003b). The medical, social and economic costs of making a diagnosis in those not at increased risk must be balanced against the costs of failing to diagnose those at increased risk.

Historically, this threshold was determined by the relationship between blood glucose levels and microvascular complications in type 1 diabetics: however, it may be more important that this threshold is determined by the relationship between blood glucose levels and macrovascular risk in a wider population (i.e. those with either impaired glucose tolerance or type 2 diabetes).

The WHO and other bodies have adopted the ADA’s diagnostic criteria (The Expert Committee 1997), but there have been different recommended optimal methods of diagnosis. The WHO prefers the OGTT, supported by evidence that 2 hour post-load plasma glucose levels were more accurate than fasting plasma glucose levels in identifying those at increased risk of death associated with hyperglycaemia (DECODE 1999). The drawback of ADA’s preference for fasting plasma glucose levels is that “normal” results carry the risk of missing some diabetics, especially among the elderly and in some ethnic groups: the earliest defect in the natural history of beta cell dysfunction is the reduction of first-phase insulin release, associated with 2 hour post-load hyperglycaemia.

Although diabetes is “arbitrarily” and solely diagnosed on the basis of blood glucose levels, it should be regarded as a syndrome that includes other metabolic and haemodynamic features.

DISEASE PROCESSES OF TYPE 2 DIABETES MELLITUS

DEFECTS RESPONSIBLE FOR TYPE 2 DIABETES

The chronic hyperglycaemia of type 2 diabetes results from diverse and progressive disease processes that cause:

In type 2 diabetes, both of these defects coexist and both can be caused by a plethora of genetic or environmental factors. Most commonly, type 2 diabetes appears to be inherited as a polygenic trait, with environmental factors also involved, often at a very young age.

Secretion of insulin, in response to rising blood glucose levels, occurs in two phases in healthy individuals:

Early in type 2 diabetes, β-cells begin to lose their initial response of increased insulin secretion (“first phase”). Sustained hyperglycaemia reduces β-cell function by “glucose toxicity”. With progression of the disease, the loss of first-phase secretion leads to early post-prandial hyperglycaemia, exaggerated late (“second-phase”) insulin secretion and late post-meal hypoglycaemia. Insulin secretory pulses become abnormal under basal conditions. The loss of first-phase insulin secretion, which leads to post-prandial glucose “spikes”, is associated with an increased risk of cardiovascular disease.

In insulin resistance, insulin is unable to produce its usual effects at concentrations that are effective in normal individuals. Its onset precedes the development of type 2 diabetes and may arise from a variety of genetic mutations. It is thought that the reduced action of insulin is linked closely with the cardiovascular risk factors, such as obesity, that are part of the insulin resistance syndrome (Reaven 1988).

Malnutrition in utero and during early infancy may be associated with an increased risk of developing type 2 diabetes later in life (the “thrifty phenotype” hypothesis) by affecting both β-cell function and insulin resistance. Regular physical exercise, when undertaken consistently from childhood, can protect against type 2 diabetes by improving insulin sensitivity.

BIOCHEMISTRY OF DIABETES COMPLICATIONS

Vascular tissues are freely permeable to glucose. Poor glycaemic control renders such tissues more vulnerable to insult, which starts insidiously and may eventually lead on to the failure of major systems. Abnormalities may occur in endothelial cells, vascular smooth muscle cells, glomeruli and mesangial cells, and cardiomyocytes. The clinical consequences of diabetic microvascular disease include visual impairment, chronic renal failure and neuropathic foot ulceration.

Four main mechanisms (not mutually exclusive) have been implicated in the pathogenesis of glucose-mediated vascular damage:

However, clinical complications are driven by raised blood pressure, dyslipidaemia and multiple other abnormalities, particularly those that contribute to insulin resistance. Some of these precede the onset of type 2 diabetes, by which time atheromatous changes have already been established. This is why prevention or early detection is important.

The precise pathogenesis of atheromatous change in patients with diabetes may vary not just between individuals, but also between sites and different calibre of arteries in the same individual. A better understanding of these mechanisms may help to identify potential therapeutic interventions, although lifestyle modification and vigorous correction of raised blood pressure and dyslipidaemia must remain central to reducing cardiovascular risk.

INTERMEDIATE HYPERGLYCAEMIC CONDITIONS

The term “pre-diabetes” has been used to categorise people with impaired glucose metabolism, but who are not diabetic. Many, but not all, progress to diabetes. The WHO term “intermediate hyperglycaemia” may be more accurate. Whichever term is used, identification followed by appropriate interventions (particularly aimed at optimising lifestyle) can achieve real benefit for this group.

IMPAIRED GLUCOSE TOLERANCE AND IMPAIRED FASTING GLUCOSE

These terms are not interchangeable and do not define identical groups of individuals. The rationale for establishing these intermediate categories of impaired glucose regulation is based on their value in predicting cardiovascular risk (IGT) and future diabetes mellitus (IFG).

Impaired glucose tolerance (IGT) refers to a glucose metabolic state that is intermediate between normal glucose homeostasis and diabetes mellitus. IGT only applies to a plasma glucose level in the range of 7.8 to 11.0 mmol/l at 2 hours after a 75 g glucose load. Patients can be labelled as having IGT only from an OGTT. Individuals with IGT are at increased risk of developing macrovascular disease. IGT progresses to type 2 diabetes in 37% at 5 years (Gillies 2007) and 50% at 10 years (Davies 2006). It is logical to regard IGT as a risk factor rather than as a disease entity, particularly as many individuals with IGT are asymptomatic and have normal plasma glucose levels in their daily lives. Some evidence suggests that the most cost-effective interventions to prevent or delay the onset of diabetes should target individuals with IGT, followed by high-risk groups.

Impaired fasting glucose (IFG) applies only to a fasting plasma glucose level in the range between a lower limit of 6.1 mmol/l (recommended by JBS2, WHO and the IDF) and an upper limit of 6.9 mmol/l. Some patients, particularly elderly or Indo-Asians, can have IFG, but fulfil the diagnostic criteria for diabetes because their 2 hour post 75 g load plasma glucose level is 11.1 mmol/l or greater. Thus, patients with IFG can have either diabetes or IGT or normal glucose homeostasis (based upon the 2 hour result). This has major implications for screening, because a fasting plasma glucose level below the diagnostic threshold for diabetes does not exclude current diabetes.

If IFG is defined as between 6.1 and 6.9 mmol/l, then it includes a much lower proportion of the population than is categorised as having IGT. One review found that of those who had IFG and/or IGT, 16% had both, 23% had IFG alone, and 60% had IGT alone, with significant age and gender differences between the glucose intolerance categories (Unwin et al 2002). IFG and IGT may be different metabolic states. Although the ADA has recommended a reduced lower limit for IFG to 5.6 mmol/l is, on balance, a better predictor for cardiovascular and metabolic outcomes (The Expert Committee 2003a), other guidance (WHO/IDF, JBS2, NICE/NSF still recommends that the lower limit should remain at 6.1 mmol/l (WHO/IDF 2006).

There has been considerable research into the factors that increase the likelihood of an individual with intermediate hyperglycaemia developing diabetes. It is also interesting to look earlier in the natural history at factors that may cause glucose intolerance. Smoking is thought to increase insulin resistance, but the evidence is inconclusive as to whether smoking is an independent risk factor for the development of diabetes. The CARDIA study found that, in young individuals with normal glucose tolerance, both active and passive smoking were associated (more so in whites) with the development of glucose intolerance (Houston et al 2006).

METABOLIC SYNDROME

Insulin resistance is associated with a collection of abnormal risk factors (obesity, impaired glucose tolerance, hypertension and dyslipidaemia) and is now recognised as a major underlying contributor to increased coronary heart disease (CHD) mortality. Metabolic syndrome is a defined cluster of abnormal cardiovascular risk factors; it doubles cardiovascular disease (CVD) mortality, trebles the onset of CVD events (Carr et al 2004), and predicts the development of not only type 2 diabetes, but also obstructive/sleep airways disease, gall stones, some cancers and chronic kidney disease.

The two major previous definitions of metabolic syndrome were from:

In 2005, the International Diabetes Foundation (IDF) proposed a new definition for metabolic syndrome for clinical use (set out in Table 1.4) that avoids the technical difficulties associated with insulin measurement (International Diabetes Federation 2005).

TABLE 1.4 International Diabetes Federation (IDF) definition of metabolic syndrome (IDF 2005)

Parameter Qualifications
In all cases:
Central obesity (waist circumference)

 

Any 2 of the following 4: Raised triglyceride level Reduced HDL-C levels Raised blood pressure Raised fasting plasma glucose

OGTT: oral glucose tolerance test

Epidemiological data about the metabolic syndrome are not entirely reliable due to the use of different definitions, but the prevalence varies amongst different ethnic groups, ranging from 22 to 39% of the adult population. It is commoner in an Indo-Asian population: a BMI greater than 23 kg/m2 in Indo-Asians (as compared to 25 kg/m2 in white Caucasians), is now thought to indicate increased CVD risk in this population, subject to the occasional confusion of obesity with being overweight (Hanif et al 2002).

Although the presence of metabolic syndrome does “predict” CVD events, there is no evidence that its criteria enhance the estimation of CVD risk in either diabetic or non-diabetic populations beyond existing tools, such as the New Zealand tables. However, the criteria associated with metabolic syndrome, particularly increased waist circumference, are better predictors of the development of type 2 diabetes (Sattar 2006).

Although no data are yet available from any large intervention trials in primary care for preventing or delaying diabetes or CVD in people with metabolic syndrome, there are good reasons for managing metabolic syndrome aggressively, addressing all relevant cardiovascular risk factors:

PREVALENCE OF TYPE 2 DIABETES

FACTORS THAT AFFECT THE PREVALENCE OF TYPE 2 DIABETES

Deprivation

Deprivation is associated with a higher prevalence in both sexes aged 35 to 74 years (Newnham et al 2002), although it is unclear whether this is independent of the above factors. The PBS model estimated the prevalence of diabetes to be 35% higher than the mean in the most socio-economically deprived fifth of the English population.

CONSEQUENCES OF TYPE 2 DIABETES MELLITUS

DIABETIC CONTROL, MORTALITY AND COMPLICATIONS

The diagnosis of type 2 diabetes mellitus has a profoundly adverse effect on morbidity and mortality. The long-term complications are mostly commonly vascular in origin and can be divided into macrovascular (ischaemic heart disease, cerebrovascular disease, and peripheral arterial disease) or microvascular (retinopathy, nephropathy and neuropathy).

In its 2004 report, Diabetes UK listed some truly frightening statistics (Diabetes in the UK 2004):

Overall, 5-year mortality in type 2 diabetics increases two- to threefold and age-adjusted life expectancy is reduced by 5 to 10 years compared to the general population (Panzram 1987), with cardiovascular disease being the predominant cause of mortality.

The adverse effects of sustained hyperglycaemia and poor management on mortality and morbidity in type 2 diabetes have been studied extensively. The UKPDS has now identified poor glycaemic control among the risk factors for coronary artery disease in type 2 diabetics (Turner et al 1998). The UKPDS also demonstrated that improving glycaemic control significantly reduced the risk of microvascular complications (e.g. retinopathy, nephropathy), with lesser reductions in macrovascular disease (e.g. CHD, major stroke) and no effect on diabetes-related mortality in type 2 diabetics (UKPDS 1998a, Stratton et al 2000).

As many type 2 patients at diagnosis have complications, particularly vascular, and/or adverse cardiovascular risk factors, early diagnosis (including targeted screening) and high-quality management can improve their future well-being.

FINANCIAL CONSEQUENCES OF TYPE 2 DIABETES

Several attempts have been made to ascertain precisely how much is spent both directly and indirectly on diabetes care.

In 2002, the Diabetes NSF estimated that the NHS spent £3.5 billion per year on treating diabetes and its complications (Department of Health 2002). Since then the actual costs will have increased, due to economic and health-care inflation and to the rising prevalence of type 2 diabetes. T2ARDIS estimated that diabetes was responsible for 5% of the total NHS expenditure (British Diabetic Association 2000). The prevalence of type 2 diabetes, with its associated morbidity and mortality, continues to increase, as do its costs and the pressures on those responsible for financing health care. Diabetes UK predicted that the proportion of NHS expenditure on diabetes will rise to 10% by 2011 (Diabetes in the UK 2004).

The UKPDS calculated the annual manpower cost of implementing its findings for glycaemic and blood pressure control in patients with type 2 diabetes to be £264 per patient in 1998 (UKPDS 1998a, b).

The Type 2 Diabetes: Accounting for a major Resource Demand in Society in the UK (T2ARDIS) project looked at the financial impact of type 2 diabetes and presented its results to Diabetes UK’s Annual Professional Conference in March 2000 (British Diabetic Association 2000). T2ARDIS calculated that the average annual cost of treating each person with type 2 diabetes incurred direct costs to the country of £2152, comprising:

T2ARDIS also showed that the presence of both microvascular and macrovascular complications in an individual increased the average NHS costs in the calculation above fivefold, personal expenditure threefold, and social services costs fourfold.

Published in 2002, the CODE-2 study gathered data on 7000 type 2 diabetics from eight European studies: it estimated the average annual cost per patient to be £1934, of which 55% could be attributed to hospital admissions and 7% to the cost of blood glucose-lowering medication (Jonsson 2002); these estimates are not too dissimilar to T2ARDIS.

At Diabetes UK’s Annual Professional Conference in April 2005, Professor Rhys Williams presented predictions that, by 2025, diabetes care worldwide could cost between US$153 and 286 billions, accounting for 7.5 to 13.5% of total health-care costs: a terrifying prospect.

Wanless estimated that the additional annual cost of implementing fully the Diabetes NSF in England by 2010–2011 would be £600 million; however, an annual saving of £200 million would result from measures that reduce the medical effects of diabetes (by prevention, earlier detection or improved care to reduce complications).

SCREENING FOR TYPE 2 DIABETES MELLITUS

HOW STRONG IS THE CASE FOR SCREENING FOR TYPE 2 DIABETES?

Since setting up and implementing any screening programme can be a major undertaking with considerable costs, it is necessary to be able to evaluate the benefits of any proposal against recognised criteria (Davies 1997, The Expert Committee 2003a). The role of the National Screening Committee (NSC) is to provide advice about established and newly proposed screening programmes, with the aim of evaluating these against specified criteria, published in 1998 and divided into four areas: the condition, the test, the treatment and the screening programme (National Screening Committee 1998).

While the NSC crirteria are primarily designed to evaluate the cost-effectiveness of a screening programme, it may be more useful at practice level to evaluate the benefits of screening against established and recognised criteria (The Expert Committee 2003a). These can be summarised as follows:

At least one-third of patients with type 2 diabetes have at least one complication present at diagnosis (UKDIABS 2000). However, type 2 diabetics identified by screening have:

Patients found to have IGT may benefit from interventions to reduce both their risk of becoming diabetic in the future and of their existing propensity to develop cardiovascular disease. Ultimately, the practice must be able to offer high-quality, appropriate and effective care on a consistent basis to newly diagnosed diabetics.

Diagnosis should not cause physical harm. There are numerous interventions in diabetes for which the benefits outweigh harm, although any intervention carries some degree of risk.

7. Case finding and treatment must be cost-effective, in relation to health expenditure as a whole.

This is unlikely if screening the general population solely for diabetes (Goodyer 2006). In addition to a lower yield of new cases, whole-population screening requires considerable resources. One study calculated the workload as 1 hour per week for a year to screen 620 patients during that period (Lawrence et al 2001). However, a screening programme that recruited well elderly Americans found that the presence of certain factors (age, gender, ethnicity, raised BMI, greater waist:hip ratio, hypertension) increased the yield to as much as one new case of diabetes diagnosed for every six individuals screened (Franse et al 2001).

Targeted screening of “high-risk” groups would require less resource and produce a higher yield (thus, be more practical) than screening the whole population. If additional information needed to estimate cardiovascular risk was gathered at screening, then all screened individuals, even the majority who screen negative for diabetes, could benefit from this estimation, particularly if interventions are available to reduce this risk.

It should not merely be an isolated one-time effort. Depending upon what the National Screening Committee recommends, any screening programme will need to be managed, with an agreed set of quality assurance standards. Primary care is well placed to develop the accurate population and disease registers required to identify at-risk subjects, and to undertake regularly both recall and screening tests, provided that adequate systems are in place and maintained.

In 2001 it was argued that the case for whole-population screening for diabetes could not be made (Wareham & Griffin 2001). In the light of current evidence, the case for a cost-effective screening programme can be made only if either:

PRACTICAL ISSUES IN SCREENING FOR TYPE 2 DIABETES

Any practice seeking to screen a population for type 2 diabetes needs to consider its answers to five practical questions:

Additional evidence is required to resolve fully the uncertainties that surround the first three questions, a point recognised by the Diabetes NSF.

THE LIKELY FUTURE SHAPE OF DIABETES SCREENING PROGRAMMES

The Diabetes Heart Disease and Stroke (DHDS) Project was set up to explore these practical issues. In its 2006 report, the overall “pick-up” rate for newly diagnosed diabetics was 4.3% of those screened (Goodyer 2006), but the rate varied, being higher in those populations where the prevelance of diabetes is greater. Although the project did not evaluate cost-effectiveness, the results do not support this in a screening programme searching solely for new cases of diabetes in a general population; rather, the screening for diabetes in a general population is best incorporated into a general vascular risk assessment.

This point both informs and underlies the Department of Health’s 2006 White Paper (DoH 2006) which proposes health MOTs at various stages of life. At the time of writing, a diabetes screening programme is unlikely to stand alone, but would be incorporated into a population-wide assessment, probably at significant age milestones (i.e. 40, 50 and 60 years), of parameters (that may include waist circumference, blood pressure, fasting lipids and glucose) which will identify a subset with metabolic syndrome that may need more frequent (every 3 years?) fasting blood glucose checks.

Ultimately, any systematic and sustained programme requires sufficient additional resources for screening, diagnostic tests and treatment; and their provision must be balanced against other demands made upon the practice. A practice’s decisions need to be based upon what is most feasible, both logistically and clinically.

PREVENTION OF TYPE 2 DIABETES MELLITUS

POSSIBLE INTERVENTIONS TO PREVENT TYPE 2 DIABETES: EVIDENCE BASE

A number of published studies demonstrate that type 2 diabetes in high-risk individuals can be prevented either by improving lifestyle or by prescribing medication.

Modifying lifestyle

The Da Qing IGT and Diabetes Study (China), which followed up individuals with IGT over 6 years, showed a reduction by at least one-third of the incidence of new diabetes with either diet or exercise interventions or both (Pan et al 1997).

The Finnish Diabetes Prevention Study Group, followed up overweight individuals with IGT over a mean of 3.2 years, and compared “individualised” counselling aimed at reducing weight, modifying diet and increasing physical activity against controls. The cumulative incidence of new diabetes was reduced by 58% in the intervention group, or one case of diabetes was prevented for every 22 overweight individuals with impaired glucose tolerance “treated” for 1 year (Tuomilehto et al 2001). The benefits were sustained (APR 3.1%; RRR 43%) during a median follow-up of 3 years after the intervention was discontinued (Lindstom 2006).

The Diabetes Prevention Program (DPP) in the USA, followed up “high-risk” subjects over a mean of 2.8 years, and compared three arms: standard lifestyle recommendations plus placebo, standard lifestyle recommendations plus metformin, and an intensive programme of lifestyle modification (16 lessons covering diet, exercise and behaviour modification). The reduction in incidence of new cases of diabetes was 31% in the metformin group (treat 41.7 subjects for 1 year to prevent one new case) and 58% in the intensive programme group (treat 20.7 subjects for 1 year to prevent one new case) (Diabetes Prevention Program Research Group 2002).

To apply any of the above programmes on a sustained basis to a large population will require considerable effort and resources. However, the evidence does support modifications of lifestyle:

with the aim of achieving and maintaining weight reduction, which has considerable health benefits beyond preventing type 2 diabetes.

Medication

Any drug shown to be effective in preventing diabetes could potentially create a huge market for pharmaceutical companies. Even if proved effective, the colossal financial costs of treating large populations with some of these drugs may be prohibitive.

The following studies investigated drug therapy to prevent diabetes using different classes of glucose-lowering agents:

In addition:

Finally, there are data to suggest that blockade of the renin-angiotensin system may prevent diabetes:

An incidental finding in the Heart Outcomes Prevention Evaluation (HOPE) trial was the lower rate of new diagnosis of diabetes in vascular high-risk patients aged over 55 years treated with the ACE inhibitor ramipril (Yusuf et al 2001). In the Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) study, rosiglitazone, unlike ramipril when compared to placebo, reduced significantly (hazard ratio 0.40, 95% Cl 0.35–0.46) the risk of patients with impaired fasting glucose or IGT developing diabetes. Although the study was well conducted, the results need to be interpreted and applied with caution, as rosiglitazone did increase fluid retention and heart failure and it is still an expensive drug being used to treat here something for which changes in lifestyles are still the mainstay.

The HOPE and LIFE studies found that inhibition of the renin-angiotensin system may improve glucose tolerance. The LIFE study authors suggested an effect on insulin resistance, but other hypotheses suggest an increased insulin secretory response, either by inducing a raised pancreatic islet blood flow to secure a better early insulin response (Carlsson et al 1998) or as a result of the higher serum potassium levels associated with ACE-inhibitor use augmenting insulin secretion (Santoro et al 1992).

However, a recent systematic review concluded that, despite data that some drugs lowered the incidence of diabetes compared to placebo, no single pharmacological intervention can be definitively recommended for diabetes prevention. Further research is needed, using studies designed with the incidence of diabetes as the primary outcome and of sufficient duration to differentiate between real prevention and the delay or masking of the condition (Padwal et al 2005). Whilst the benefits of lifestyle changes may last beyond the period of intervention, it is unclear whether the benefit of medication is sustained. Although evidence supports the effectiveness of both lifestyle and pharmacological interventions in reducing the risk of IGT progressing to type 2 diabetes (Gillies 2007), selecting the optimal intervention requires careful consideration of benefit vs. harm, patient preference, likely concordance, available resources and other issues that are, as yet, unresolved.

DEVELOPING POLICIES THAT TACKLE PREVENTION: ISSUES THAT NEED TO BE CONSIDERED

Societies and their health services will need to look at implementing a range of measures targeted at individuals to whole populations. Successful health education requires collaboration between disparate agencies with a unity of purpose, from appropriate government policies down to practice level. Health professionals have an important role, but are not the only players here. Government policy is reflected in Chapter 6 of the NSF Diabetes’ Strategy, which refers to national initiatives and best-practice models that tackle diet, physical activity and smoking cessation, particularly in schools and/or deprived areas (DoH 2002).

The huge demand placed upon finite resources (financial and human) is one of the main barriers to applying and sustaining successfully any of the above interventions to a large population. The practical compromise may be to give priority to proven interventions in those individuals most likely to benefit.

Attempts to change an individual’s behaviour raise the potential dilemmas that surround patient empowerment. The concept is laudable and may often enhance effective disease management; however, individuals have the right to make choices that ultimately may cause them harm. Lifestyles are largely the result of choices made by individuals. Any intervention to alter these must respect each individual’s right to make decisions and must assess each individual’s willingness to change.

Another challenge for health professionals and organisations is to develop clear and equitable policies in response to patient demands for available interventions that may lack full clinical justification or affordability within a limited budget.

KEY POINTS