Which type of prevention strategies would be considered for a patient diagnosed with diabetes?

Need for prevention and prevention strategies

Type 2 diabetes is one of the most rapidly increasing chronic diseases in the world. The need for its primary prevention has been increasingly emphasised, although only during the past 10–15 years1–6. The main justifications of prevention of type 2 diabetes are the possible prevention or postponement of complications related to type 2 diabetes in order to reduce both human suffering and the socio-economic burden on the community. It has been repeatedly shown that both symptomatic and asymptomatic diabetic patients have an increased prevalence of both macrovascular and microvascular complications by the time the disease is first diagnosed7–9. A Swedish study showed that 77% of all costs for the care of type 2 diabetes were due to its complications, mostly cardiovascular10. Also, in people with impaired glucose tolerance (IGT), both mortality and the risk of cardiovascular disease are markedly increased11,12. It has been estimated that at the time of diagnosis of clinical type 2 diabetes only 50–60% of the pancreatic β-cell capacity is left, due to the fact that the disease process has already existed for more than 10 years13. Therefore, the optimal (and probably the only effective) strategy to reduce the increased burden of type 2 diabetes is primary prevention, i.e. to tackle the worsening of glucose intolerance before harmful effects of hyperglycaemia become permanent.

The increased knowledge about the aetiology, pathogenesis and natural history of type 2 diabetes has lead to primary prevention becoming a reality. Although an unequivocally accepted consensus regarding the early pathogenesis is still lacking, preventive measures can be based upon the best current available knowledge. The rapidly increasing number of patients with type 2 diabetes, the severity of the disease, its multiple and severe complications and the increasing socio-economic costs emphasise the importance of immediate preventive actions. The current situation for type 2 diabetes can be compared with the epidemic of coronary heart disease during the 1960s and 1970s in many industrialised countries14–16. Primary preventive measures targeted at the known modifiable risk factors of coronary heart disease have shown to be successful. Both the incidence and mortality of coronary heart diseases and stroke have halved in about 20 years, though the extent to which this reflects the success of preventive policies is not known17.

Primary prevention of type 2 diabetes can be defined as all measures designed to reduce the incidence of the disease on the population level, by reducing the risk of its onset. This may be achieved by modifying the underlying risk factors for type 2 diabetes. Secondary prevention of type 2 diabetes can be defined as all measures designed to reduce morbidity and mortality among diagnosed type 2 diabetic patients.

Prevention strategies

Since type 2 diabetes is a heterogeneous and multifactorial disorder, preventive measures must be based upon modification of several risk factors simultaneously. Otherwise, the potential for prevention remains incomplete and insufficient. The existing evidence, however, suggests that even a single intervention, e.g. increased physical activity in sedentary people or weight loss in the obese, can lead to a marked reduction in the risk of type 2 diabetes18,19 There are two components to the design of a prevention strategy: (i) a population-based strategy, for altering the life-style and those environmental determinants which are the underlying causes of type 2 diabetes in the entire population; and (ii) a high-risk strategy for screening individuals at high risk for type 2 diabetes and bringing preventive measures to this group on an individual basis.

The basic underlying principle of the population approach is to shift the average blood glucose concentration of the whole population in the direction of lower values, or to prevent the increase in blood glucose with age. The population strategy and the high-risk strategy are, however, complementary and one of them may not be effective without the other being applied simultaneously. The primary emphasis on the population approach may be more appropriate in societies with a particularly high susceptibility to type 2 diabetes, while the emphasis on the high-risk strategy may be more appropriate in communities with a moderate risk. Since the frequency of the disease is increasing steeply in most populations in the world, the population approach needs to be considered as a priority.

According to present knowledge, the known high risk individuals are: (i) those with a family history of type 2 diabetes; (ii) women who had gestational diabetes; (iii) people whose blood glucose has been previously found to be moderately increased; and (iv) hypertensive subjects. In addition, obese and physically inactive people have an increased risk for type 2 diabetes. Altogether, these high-risk individuals are so numerous in modern societies that they would in fact comprise a large proportion of the adult population world-wide. As knowledge of the genetic predisposition for type 2 diabetes increases, communities with a high genetic predisposition should be targeted.

Natural history of type 2 diabetes – the basis for prevention

Primary prevention of type 2 diabetes depends on our current knowledge of the natural history of the disease. It is known that type 2 diabetes has a strong genetic predisposition4. In addition, recent findings point towards the importance of events during fetal life and infancy. It has been hypothesised that fetal experience, such as malnutrition, can lead to programming of the metabolic profile that will contribute to the development of chronic diseases in adult life, including type 2 diabetes20. This early programming mimics to a great extent ‘genetic’ transmission of diseases. When predisposed individuals become more insulin resistant, for example due to obesity or physical inactivity in their adult life, they usually develop some degree of glucose intolerance. When the pancreatic β-cell capacity is no longer sufficient to compensate for the increasing insulin production needed to overcome insulin resistance, hyperglycaemia worsens and overt diabetes develops. It is important to understand that progression through these stages is not inevitable – it is probable that this progression can be halted and actually was halted in years past when populations were less obese and more physically active. Potentially, intervention at any stage of the natural history of diabetes may prevent the progression to a later stage of glucose intolerance.

When does the clock start ticking for type 2 diabetes?

The clock starts ticking for diabetes long before any abnormalities can be detected. A number of stages relating to the course and development of type 2 diabetes may be defined. The data from the UK prospective diabetes study showed that, at the time of the diagnosis of type 2 diabetes, 50% of the overall β-cell function had already been lost13. From the further linear deterioration of the β-cell capacity in these diabetic patients, it was estimated that the β-cell capacity had begun to decline ∼12 years prior to the clinical diagnosis of diabetes. The first stage in this process is genetic susceptibility. Another very early component that may contribute to the predisposition is the disproportionate body size at birth, that is thinness or macrosomia at birth. These can be readily identified and may be considered as the first identifiable risk indicator, especially in families with a history of diabetes. In the general population, however, general cut-off points for thinness or fatness vary within populations and have yet to be defined.

It is well established that an abnormal intra-uterine environment leads to structural and functional adaptations in the fetus which have long-lasting consequences for its metabolism in later life. A thesis of this book is that a thrifty phenotype develops in which inadequate fetal nutrition programmes impaired development of glucose and insulin metabolism in adulthood21. Disproportionate size at birth is a fairly recently discovered risk factor in the list of risk factors for type 2 diabetes. The proposed biological mechanisms involve both pancreatic β-cell dysfunction and insulin resistance; therefore, the associations are highly plausible given the multiple observational studies and animal experiments that support them.

British studies originally showed that babies born with the lightest birth weight, i.e. < 2.5 kg, were almost 7 times more likely to have some degree of impairment in their glucose tolerance compared with those born heavier22. Similar findings have now been made globally in a variety of populations and ethnic groups23–25. In keeping with the thrifty phenotype hypothesis are also findings from twin studies; the twin with type 2 diabetes has lower birth weight26. Monozygotic twins share the same genetic make-up, suggesting that the mechanism of the link between low birth weight and subsequent type 2 diabetes is environmental. This should not lead to the conclusion that the there is no role for genetics in the development of type 2 diabetes, but it certainly shows that the link between low birth weight and type 2 diabetes can occur independently of a genetic influence. The thrifty phenotype hypothesis has been challenged by McCance and co-workers who described a U-shaped relationship between birth weight and type 2 diabetes among Pima Indians27. The risk of type 2 diabetes in infants weighing <2.5 kg at birth was 3.8 times that of infants weighing 2.5–4.5 kg whereas those with birth weights >4.5 kg had a 1.8-fold increased relative risk. The increased risk associated with higher birth weight could in fact be due to the high prevalence of type 2 diabetes among the Pima Indians and consequently high prevalence of gestational diabetes and macrosomia in the offspring.

The importance of exposures before birth on the life-time occurrence of chronic diseases has recently been shown in many populations and for many diseases20. In the past, when infectious diseases were more common, it was evident that childhood health affected health in adult life. Now the current observations also stress the importance of fetal life as a crucial period for the natural history of type 2 diabetes.

Growth in childhood and adolescence

The thrifty phenotype hypothesis suggests that the fetal nutritional environment has a programming effect on various physiological functions including glucose and lipid metabolism and blood pressure20. It is the mismatch between a relatively poor intra-uterine environment and a nutritionally rich environment in later life that increases the risk of diabetes and other diseases. Adaptation to undernutrition in utero may limit the extent of dietary change to which a generation can be exposed without adverse effects. Individuals exposed to undernutrition in utero are more susceptible to type 2 diabetes if they catch-up in weight and body mass index (BMI) during childhood as shown by a recent study in Finland25. Since children born small and thin have proportionally less muscle mass, catch-up growth would mean disproportionate increase in weight and fat mass in relation to muscle and height during early childhood. Therefore, prevention of obesity during childhood is important among children born small and thin.

Recently, an alarming rise in the incidence of type 2 diabetes among children and adolescents in the US has been observed, though this is not limited to North America28,29. As the young population world-wide is becoming increasingly overweight and sedentary, type 2 diabetes will probably appear more frequently in younger age groups than before. Puberty appears to play a major role in the development of diabetes in children. During puberty, there is increased resistance to the action of insulin, resulting in hyperinsulinaemia which contributes to the manifestation of both type 1 and type 2 diabetes. One underlying cause of this could be increased growth hormone secretion, and this effect is modified by obesity20. It is commonly understood that subjects with an early-onset type 2 diabetes probably have a stronger genetic predisposition than those diabetic patients whose onset age is older. The recent increase observed in the prevalence of type 2 diabetes in younger age groups has, however, occurred too rapidly to be the result of an increased gene frequency and altered genetic pool, emphasising the importance of environmental factors that can trigger the disease onset in genetically predisposed people.

Health habits and their ‘programming’ in youth

Another important aspect of fetal programming is the ‘programming’ of life-style. Children readily adopt the life-style of their parents. Childhood and adolescence are periods in life during which they also tend to adopt the life-styles of their peers. This is the first period when knowledge and awareness of type 2 diabetes and its risk factors should be disseminated to the population. Primarily, the preventive message should include aspects related to practical advice regarding a healthy diet and the promotion of physical activity; it should be targeted to the entire population, not only to high risk individuals. The ‘peer pressure’ among the youth is so strong that benefits expected from such a population approach to control environmental risk factors for type 2 diabetes are likely to be substantial.

Adult life-style

The epidemic of obesity can be viewed as the result of a normal response to an abnormal environment. In 1985, the World Health Organization named obesity the single most important risk factor for type 2 diabetes30. This is evident since it has been estimated31 that up to two-thirds of type 2 diabetes could be prevented by keeping the BMI < 25 kg/m2. The increase in obesity in adults is partly explained by a decrease in physical activity, but sedentary life-style is also an independent risk factor for type 2 diabetes4,32. The combination of ‘Westernisation’ and genetic predisposition for type 2 diabetes can result in an epidemic of type 2 diabetes even within one generation as seen in some populations such as Pima Indians and Nauruans33. Therefore, it would be necessary to set a target in the population as well as for individuals to maintain the level of body weight as it was around the age of 25 years and also to maintain a sufficient level of physical activity throughout adult life. By applying these simple measures, more than half of the cases of type 2 diabetes occurring before the age of 65 years could be prevented.

Elderly individuals

The occurrence of type 2 diabetes increases with increasing age, and the vast majority of diabetic subjects are elderly. There are physiological reasons for this and they are largely related to life-style. Muscle mass usually decreases with advanced age. To what extent this can be considered as a part of a normal ageing process and to what extent it is due to an increase in sedentary life-style with age is not fully settled. Also, various musculoskeletal problems increase with age and often affect exercise habits. It is probable that some exposures during the intra-uterine period and early infancy may prevent normal β-cell growth and replication leading to a permanently reduced β-cell capacity. The pancreatic β-cell mass decreases with age. This process is accelerated by peripheral insulin resistance due to influences such as obesity, physical inactivity, and diet. In people who are genetically susceptible to diabetes, this process leads to hyperglycaemia and, ultimately, to clinical diabetes. The tempo of this development and hence the age-at-onset of disease are obviously determined by the intensity of environmental exposure. This is well illustrated by the increasing number of type 2 diabetics among adolescents and young adults34.

Identification of target groups for intervention and implementation of preventive measures

Family history

Family history is one of the most important determinants of type 2 diabetes. The currently accepted pathogenic model for type 2 diabetes is based upon the assumption that a genetic predisposition is necessary, but not a sufficient cause, for the disease. Thus, type 2 diabetes may only develop in individuals who carry diabetes susceptibility genes. Since in some populations such as Native Americans and Pacific Islanders, the life-time prevalence of type 2 diabetes is now over 50%, it can be assumed that more than half of people in these populations are genetically predisposed to diabetes3. It has been suggested that ‘thrifty genotypes’ have accumulated in such isolated populations35. Similarly, epidemiological studies from Europid populations show that 20–30% of people aged 70 years or above have type 2 diabetes36. Thus, at least this proportion of Europid populations carry susceptibility genes. Assuming a Mendelian inheritance, at least half of their siblings and offspring should also have these genes.

Twin studies have suggested that the majority of monozygotic twin pairs will become concordant for type 2 diabetes after one twin develops the disease. The concordance estimates vary between 60–100%37. Our own twin study has revealed that approximately half of the liability to type 2 diabetes is related to genetic effects and a half to environmental exposure38.

Previously, family history has not been found to be a sensitive marker for the disease for three reasons: (i) almost half of the first degree relatives of type 2 diabetic patients have not inherited the susceptibility genes; (ii) the majority of those genetically predisposed do not develop diabetes either because of low exposure to environmental risk factors or through premature mortality from other causes; and (iii) diabetic subjects in the past were often not properly diagnosed39. While the first reason is still relevant, the latter two have drastically changed, but still remain relevant. Looking at the importance of family history from the other perspective, a positive evidence for family history of type 2 diabetes is always an indication for at least a 50% probability of diabetes risk for an individual.

Low birth weight

Type 2 diabetes has been shown to be associated with intra-uterine or early childhood malnutrition. One might, therefore, predict that the incidence of type 2 diabetes will fall as the nutritional status in a population and in pregnant women improves. Nevertheless, adequate fetal nutrition may not offset the effects of diabetes susceptibility genes. The protein metabolism of women during pregnancy is closely related to the glucose-insulin metabolism of the offspring, and the importance of essential amino acids in programming the fetus has been stressed. However, fetal growth is not only regulated by the availability of nutrients but by hormones, growth factors, and placental functions.

It would be helpful to know what proportion of type 2 diabetes is the result of early growth retardation. Birth weight, however, is a crude index of fetal growth and development, and there is a continuous relationship – rather than a threshold – between birth weight and the future risk of type 2 diabetes20. Furthermore, early catch-up growth and childhood obesity interact with an intra-uterine exposure making this matter complex25. Low birth weight can serve as a surrogate marker for intra-uterine exposure and is a risk factor for type 2 diabetes which should be considered at least in people with a positive family history. It would be interesting to examine the glucose tolerance status of individuals with optimal early growth. This might reveal a potential way to prevent type 2 diabetes. We do not yet know whether and to what extent improvements in the body compositions and diets of young women can contribute to the primary prevention of type 2 diabetes in their offspring.

Childhood obesity

Attempts to prevent type 2 diabetes in children should follow the same general paradigm as that recommended for the prevention of type 2 diabetes in adults. Although primary prevention efforts may be directed at high-risk individuals, the main strategy must be based up on applying prevention strategies at the population level.

Prevention of type 2 diabetes in high-risk children is predicated on the ability to identify those at increased risk and provide them with adequate service. The population approach should promote the avoidance of obesity and adequate levels of physical activity as desired norms for the entire community. These objectives may not be easy to achieve in the real world, but they are not unreasonable.

In addition to overall health promotion in the community at large, there is a need for health professionals to become involved in developing and implementing school- and community-based programmes to promote improved dietary and physical activity behaviours for all children as well as their families. School programmes should promote healthy food choices and increased physical activity.

Gestational diabetes

Gestational diabetes, or hyperglycaemia occurring temporarily during pregnancy, is associated with an increased risk of the later development of type 2 diabetes. The 15-year cumulative incidence is 35–40% or 3–5% per year40. Gestational diabetes is not only associated with an increased risk of diabetes in the mother, but with an increased risk of diabetes in the offspring (see Van Assche et al, this issue). Proper weight management and the promotion of physical activity in these women is essential in order to prevent the development of overt diabetes later in life. Women with previous gestational diabetes are one of the target groups whose glucose tolerance should be systematically monitored.

Hypertension

It is known that people with hypertension have more diabetes than normotensive subjects41,42, and the risk of cardiovascular disease in hypertensive diabetic patients is particularly high43. Therefore, it is important to determine the glucose tolerance status in hypertensive patients at regular intervals. While the control of blood pressure among patients treated for hypertension is often inadequate44, several studies have demonstrated that hypertensive diabetic patients seem to benefit especially from lowering of their blood pressure45,46.

Adult obesity

A close association between obesity and type 2 diabetes has been observed in both cross-sectional and prospective studies47–52. Even modest degrees of overweight increase the risk of type 2 diabetes. Obesity and physical inactivity are the most important potentially modifiable risk factors for type 2 diabetes. Based upon epidemiological data, it has been estimated that the risk of type 2 diabetes could be reduced by 50–75% by control of obesity and by 30–50% by increasing physical activity31. Preventive measures during adulthood should primarily focus on weight management and increase in physical activity.

Transiently or slightly elevated blood glucose

In general, there are a number of stages relating to the course and development of type 2 diabetes. The earliest stage of detectable abnormality in glucose homeostasis is impaired glucose tolerance (IGT), i.e. elevated postprandial blood glucose concentrations53. According to different studies, 2–5% of people with IGT will develop frank diabetes. Though a large proportion of people with IGT will have normal glucose tolerance on a repeat test54, it has been shown that many of them will later on have IGT again and will ultimately develop diabetes55; however, progression is not inevitable. The probability in worsening from IGT to diabetes is related to life-style factors such as obesity and physical inactivity. From the prevention point of view IGT is a critical stage in the development of diabetes, because it is readily detectable and treatment may prevent or delay its progression.

Past experience from primary prevention of diabetes mellitus

Even though primary prevention of diabetes was first proposed 80 years ago56 and more recently stressed by the WHO57, few studies have attempted to assess the value of measures aimed at controlling obesity and increasing physical activity in people with a high risk of the disease. Some intervention studies have used drugs but these studies will not be considered here since such intervention cannot be considered as primary prevention. An intervention programme based solely on life-style intervention is a natural way of preventing type 2 diabetes since the increased prevalence and incidence of the disease is mainly due to responses to a sedentary life-style and excessive food intake.

Unfortunately the published life-style intervention studies have not been properly designed or powered to give a definite answer to the question of whether or to what extent the primary prevention of type 2 diabetes is possible. However some have provided suggestive evidence that life-style changes are effective in halting the progression from IGT to type 2 diabetes. We will briefly summarise the main findings from these studies.

The feasibility of diet and exercise intervention in 217 men with IGT was assessed in the Malmö feasibility study18. The effect of exercise and diet was compared to a reference group with no intervention. The reference group consisted of men who themselves decided not to join the intervention programme. Thus, the groups were not assigned at random. By the end of the 5-year study period, 11% of the intervention group and 21% of the reference group had developed diabetes. Thus the incidence in the intervention group was a half of that in the reference group (RR, 0.5; 95% CI, 0.3–1.0). This study is important in demonstrating the feasibility of carrying out a diet-exercise programme for 5-years among volunteers.

More recently, data on the preventive effect of a diet and exercise intervention have been reported in a cluster-randomised clinical trial on 577 subjects with IGT in Da-Qing, China19. The cumulative 6-year incidence of type 2 diabetes was notably lower in the three (diet alone, exercise alone, diet-exercise combined) intervention groups, being 41–46% compared with 68% in the control group. This study did not apply an individual allocation of study subjects to the intervention and control groups; instead the participating clinics were allocated. Thus, the study unit was a clinic not a person and, therefore, the results based on individual data must be interpreted with caution. Furthermore, the study subjects were relatively lean, with a mean BMI of 25.8 kg/m2, making inferences to European obese IGT subjects difficult. Also, the rate of progression from IGT to diabetes was unusually high, more than 10% per year in the control group, which exceeds that usually reported in observational studies58.

Promising results on the treatment of obesity come from the Swedish SOS Intervention Study59. The 2-year incidence of diabetes was 30 times lower in surgically treated, grossly obese subjects compared to control subjects receiving regular care. The corresponding weight losses were 28 ± 15 kg versus 0.5 ± 8.9 kg (P < 0.0001), respectively. These results certainly suggest that severe obesity can and should be treated, and that the reduction of obesity results in a marked reduction in the incidence of hypertension, diabetes and some lipid disturbances.

There are some ‘natural’ experiments available in which ethnic groups have experienced rapid Westernization and with it rapid increase in the rates of obesity and type 2 diabetes. Therefore, it is logical to assume that by reversing these life-style changes it would be possible to prevent the development of the disease. Such a potential for reversibility has in fact been shown by elegant life-style intervention studies in Australian Aboriginals by O'Dea and co-workers60. In these experiments, when hyperglycaemic people returned to nature and lived a traditional hunter–gatherer way of life, hyperglycaemia was reversed.

Major recent life-style intervention studies

The Finnish Diabetes Prevention Study (DPS)

This was carried out between 1992–2000 in 5 clinics in different parts of Finland, aimed at preventing type 2 diabetes with life-style modification alone61–63. A total of 522 individuals at high risk of developing diabetes were recruited into the study, mainly by opportunistic screening for impaired glucose tolerance (IGT) in middle-aged (age, 40–64 years), overweight (BMI >25 kg/m2) subjects. The presence of IGT was confirmed in two successive 75 g oral glucose tolerance tests; the mean of the two values had to be within the IGT range. From previous studies, it was estimated that the cumulative diabetes incidence in such a high-risk group would be 35% in 6 years. The study subjects were randomly allocated either into the control group or the intensive intervention group. The subjects in the intervention group had frequent consultation visits with a nutritionist and received individual advice to reduce weight and dietary intake of total and saturated fat, and to increase fibre intake. They were advised to increase everyday activity and were offered supervised, circuit-type exercise sessions aiming to increase muscle mass in addition to aerobic exercise. The control group subjects were also given general advice about healthy life-style at their annual visits to the study clinic. An oral glucose tolerance test was done annually and, in the case of diabetic values, a confirmatory OGTT was performed.

During the first year of the study, body weight decreased on average 4.2 kg in the intervention group and 0.8 kg in the control group subjects (P = 0.0001). Most of the weight reduction was maintained during the second year. Also, indicators of central adiposity and fasting glucose and insulin, 2-h post-challenge glucose and insulin, and HbA1c reduced significantly, more in the intervention group than in the control group at both 1-year and 2-year follow-up examinations. At the 1-year and 2-year examinations, intervention group subjects reported significantly more beneficial changes in their dietary and exercise habits, based on dietary and exercise diaries.

A total of 86 incident cases of diabetes were diagnosed among the 522 subjects after a median follow-up duration of 3 years. Of these, 27 occurred in the intervention group and 59 in the control group. The cumulative incidence in the intervention group was 58% lower than in the control group (Fig. 1).

Fig. 1

Development of diabetes in subjects with IGT at baseline during the life-style intervention trial by the randomisation group63.

The difference between the groups became statistically significant after 2 years: 6% in the intervention group and 14% in the control group. At 4 years, the cumulative incidences were 11% and 23%, respectively. The absolute risk of diabetes was 32/1000 person-years in the intervention group and 78/1000 person-years in the control group. In men, the incidence of diabetes was reduced by 63% in the intervention group compared with the control group and in women by 54%.

According to these results, 22 people with IGT need to be treated for 1 year or 5 people for 5 years with a life-style intervention to prevent one case of diabetes. The public health implications of these results are wide. The primary prevention of type 2 diabetes is possible by a non-pharmacological intervention that can be implemented in the primary health care setting. It is necessary that such an intervention becomes part of routine preventive care in order to reduce the burden of type 2 diabetes that is reaching epidemic proportions in many countries. At the same time, it is also necessary to develop national programmes for the primary prevention of type 2 diabetes that include not only the high risk strategy but also the population strategy.

The Diabetes Prevention Program (DPP)

This was a randomised clinical trial comparing the efficacy and safety of three interventions – an intensive life-style intervention, or standard life-style recommendations combined with either metformin or placebo64. The study focused on high-risk individuals with elevated fasting plasma glucose and impaired glucose tolerance (n = 3234). The original closing date of the study was planned to be 2002. However, the study was terminated prematurely by the external data monitoring board because the data had clearly answered the main research questions65. Intensive life-style intervention, with 58% reduction in type 2 diabetes risk compared to the placebo group, was superior to the metformin group with 31% reduction in diabetes risk, and the DPP study confirmed the results obtained in the Finnish DPS study. The life-style intervention was done by special educators, not regular health personnel, and was intense. Thus, the translation of such intervention to a routine primary health care may not be easy.

The future

Primary prevention of type 2 diabetes needs to receive more serious attention than in the past. Even though the WHO Study Group in 1994 gave a strong recommendation that national diabetes prevention programmes should be set up, none has been initiated thus far. A plethora of observational data demonstrates that life-style factors including physical inactivity and obesity are increasing throughout the world and that these trends have been accompanied with the steep increase in type 2 diabetes. These unfavourable life-style patterns are not only an issue among adults but also among children and adolescents. As a consequence, the age-at-onset of type 2 diabetes has become younger, not only in special small ethnic groups like Pima Indians but in many societies in both industrialised and non-industrialised countries. The effect of these life-style patterns is particularly deleterious in those born small and thin and who had accelerated weight gain during childhood and adolescence.

Data from intervention studies in various settings provide unequivocal evidence that the risk of type 2 diabetes in high-risk individuals can be reversed. While it is useful to accumulate more information from interventions in other populations and cultural environments, the evidence for initiating intensive actions to prevent type 2 diabetes is clearly sufficient. The identification of high-risk subjects for type 2 diabetes is relatively easy; biochemical or other costly tests are not required, and most of the high-risk subjects are already regular customers of primary health care services. What is needed is the systematic approach to target life-style intervention to these individuals. This is not an easy task, but we know for instance from cardiovascular prevention programmes that such interventions are possible and efficient66.

Interventions in high-risk subjects alone will not be sufficient for the successful prevention of type 2 diabetes; it is necessary to initiate actions based on the population approach. The co-ordinated combination of the high-risk approach together with systematic population approaches are likely to be the most efficient strategy. Action is overdue and is only now being begun in some countries. The national consensus conference on diabetes control in Finland in 2000 listed the primary prevention of type 2 diabetes as the primary issue among all activities in diabetes care. A programme is currently being developed. Other countries are likely to develop similar activities in the near future. In such programmes, it is necessary to realise that the primary prevention of type 2 diabetes requires a long-term plan and must include a range of activities targeted at different age groups from fetal life to old age.

Correspondence to: Dr Jaana Lindström, Diabetes and Genetic Epidemiology Unit, Department of Epidemiology and Health Promotion, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland

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