Diabetes Research and Clinical Practice
Volume 76, Issue 3 , Pages 317-326, June 2007

Prevention of type 2 diabetes: A review

  • A. Hussain

      Affiliations

    • Department of General Practice and Community Medicine, University of Oslo, Post Box 1130 Blindern, N-0318 Oslo, Norway
    • Corresponding Author InformationCorresponding author. Tel.: +47 22850641; fax: +47 22850672.
    • ,
  • B. Claussen

      Affiliations

    • Department of General Practice and Community Medicine, University of Oslo, Post Box 1130 Blindern, N-0318 Oslo, Norway
    • ,
  • A. Ramachandran

      Affiliations

    • Diabetes Research Centre & M.V. Hospital for Diabetes, WHO Collaborating Centre for Research, Education and Training in Diabetes, No. 4, Main Road, Royapuram, Chennai 600013, India
    • ,
  • R. Williams

      Affiliations

    • School of Medicine, University of Wales, Swansea SA2 8PP, UK

Received 16 May 2006; accepted 19 September 2006. published online 30 October 2006.

Article Outline

Abstract 

One of the major public health challenges of the 21st century is type 2 diabetes. WHO estimates that by 2025 as many as 200–300 million people worldwide will have developed the disease. A distressing increase in children is perhaps the most alarming sign of something going wrong. Roughly half of the risk of type 2 diabetes can be attributed to environmental exposure and the other half to genetics. Central themes for prevention are the risk factors overweight, sedentary lifestyle, certain dietary components and perinatal factors. Overweight is the most critical risk factor, and should be targeted for prevention of type 2 diabetes especially among children and youths. Ethnicity and perinatal factors are also worth considering. Today we know that prevention helps. In the US Diabetes Prevention Programme for high risk individuals, there was a 58% relative reduction in the progression to diabetes in the lifestyle group compared with the controls. Within the lifestyle group, 50% achieved the goal of more than 7% weight reduction, and 74% maintained at least 150min of moderately intense activity each week. This review discusses different forms of prevention, and proposes first of all to target people with Impaired Glucose Tolerance with increasing activity and altering dietary factors. And secondly, population-based measures to encourage increased physical activity and decreased consumption of energy-dense foods are important, and may target school children and young people, certain ethnic groups and women with gestational diabetes.

Abbreviations: IGT, impaired glucose tolerance, SGE, small for gestational age, LBW, low birth weight, LGE, large for gestational age, BMI, body mass index

Keywords: Prevention, Type 2 diabetes, Review

 

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1. Introduction 

Type 2 diabetes is one of the major public health challenges of the 21st century. According to the WHO the occurring epidemic of diabetes is strongly related to lifestyle and economic changes [1]. WHO estimates that by 2025 as many as 200–300 million people worldwide will have developed type 2 diabetes [2]. This translates into an increase of nearly 6 million patients every year, according to statistics from the Centre for Disease Control (CDC). Diabetes is the sixth leading cause of death due to disease in the U.S., and the third leading cause among some ethnic populations [3]. South East Asian countries have the highest burden of diabetes [1], [2], and the projections of the International Diabetes Federation on the prevalence of diabetes mellitus and impaired glucose tolerance (IGT) for the year 2005 is, respectively, 7.5 and 13.5% [1], [2].

Over the past decade, there has been an alarming increase in the appearance of type 2 diabetes in children, a disease that formerly occurred almost exclusively in adults. Surprisingly, little is known about the determinants of type 2 diabetes in children and thereby prevention.

The term diabetes mellitus describes a group of metabolic disorders characterised by chronic hyperglycemia resulting either from a deficiency of insulin, or decreased ability to transduce the insulin signal, or both. Uncontrolled diabetes (chronic hyperglycemia) is associated with long-term microvascular and macrovascular damage and with dysfunction and failure of various organs, leading to atherosclerosis, blindness, renal failure and neuropathy.

Insulin resistance and beta-cell dysfunction are fundamental defects known to precede the onset of type 2 diabetes by many years. Beta-cell dysfunction starts some 10–12 years prior to the presentation of type 2 diabetes (Fig. 1). This provides us with a large window of opportunities to target these defects in order to attempt to prevent type 2 diabetes.

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2. Risk factors 

Among individuals with type 2 diabetes, roughly half of their disease risk can be attributed to environmental exposure and half to genetics [4]. The following risk factors and indicators are central themes for prevention: overweight, sedentary lifestyle, dietary components and perinatal factors including nutrition in utero (Fig. 2, Fig. 3, Fig. 4).

2.1. Overweight 

The rapid rise in the past several decades in the incidence of type 2 diabetes in both adults and youth has been largely attributed to the unprecedented rise in overweight. In the past decades, prevalence of overweight among youth has almost tripled [5]. The most recently available data in the US indicates that approximately 15% of youth aged 16–19 years are overweight, where overweight is defined as having a BMI at or above the 85th age- and sex-specific percentile.

The exact mechanism whereby adiposity relates to diabetes risk has not been established. In a recent finding adipocytokine, adiponectin, tend to be the most abundant gene product in fat tissue [6]. In contrast to all other known adipocytokines, adiponectin levels are known to be decreased in obese adults and in individuals with either type 2 diabetes or coronary artery disease [7]. Children with higher body fat stores tend to have lower levels of adiponectin and higher levels of TNF-α and IL-6 [8]. In addition to inflammatory processes, these agents are known to regulate a host of physiological processes directly related to carbohydrate and fat metabolism. Evidence is mounting that they are related to the development of obesity complications such as diabetes and atherosclerosis which are related to obesity [3], [9].

2.2. Food habits 

Intake of dietary energy in excess of expenditure will result in weight gain and depending on the degree and type of weight gain, increased risk of type 2 diabetes. Abundancy of cross-sectional data that support the premise dietary fat is positively associated with obesity and is therefore is a risk factor for type 2 diabetes [18], [19].

Traditionally, low-fat diets (which are relatively high in carbohydrate) have been recommended for prevention and treatment of type 2 diabetes. More recently, it has been argued that a higher fat/lower carbohydrate diet may reduce insulin resistance without untoward effects on serum lipids and cardiovascular disease risk [20].

High mono-unsaturated fat intake may improve glycemic control, and high n−3 polyunsaturated fatty acids may improve plasma triglycerides [21], but the mechanisms whereby the type of dietary fat may modulate diabetes risk have not been established.

Various micro-nutrients have been shown to affect glucose and insulin metabolism. For example, minerals such as magnesium, calcium, potassium, zinc, chromium and vanadium have been shown to reduce insulin resistance [21].

2.3. Sedentary lifestyle 

In adults, inactivity has been identified as a risk factor of type 2 diabetes, independently of effects on body size [10]. Regular physical activity reduces the risk of type 2 diabetes in adults by 20–60% in a dose-response manner [11]. Physical activity of moderate and vigorous intensity and duration is associated with decreased risk conversion of impaired glucose tolerance to diabetes, even in the absence of significant weight loss, and independently of other identified risk factors [12], [13], [14].

Low levels of physical activity and high levels of inactivity during childhood are related to increased risk of overweight [5], and physical activity interventions have been shown to be effective in reducing both visceral and total adiposity among obese adolescents [15]. Independently of an influence on body weight and composition, physical activity enhances glucose uptake by skeletal muscle cells by increasing translocation of glucose transporting protein (GLUT 4) from intracellular vesicles to the plasma membrane, improved insulin-mediated muscle blood flow, non-oxidative glycolysis, and glucose storage as muscle glycogen. Importantly, muscle contraction stimulates glucose uptake by a mechanism that is distinct from the insulin-stimulated phosphoinositol-3-kinase pathway [16]. In addition, physical activity increases glucose uptake by adipose tissue and increases insulin sensitivity and glucose storage by the liver [17].

2.4. Small for gestational age 

Fetal under-nutrition and being born small for gestational age (SGA) have been identified as risk factors of type 2 diabetes among both adults and youth [8], [9]. Low birth weight (LBW; birth weight <2.5kg) is a significant etiologic factor in the development of type 2 diabetes [22].

In a study of white children, only SGA children who were relatively heavy had reduced insulin sensitivity. Those who were relatively thinner had a mean insulin sensitivity similar to children born at appropriate weight for gestational age [23]. However, in a study of 5–29 year old Pima Indians, those who were born with LBW were thinner, yet more insulin resistant relative to their body size than those born with normal birth weight [24]. The risk of insulin resistance syndrome has also been found to be higher in African–American than white children with LBW [25]. These findings suggest that the consequences of LBW may differ by ethnicity. In a large population-based study, birth weight was found to be inversely related to the risk of gestational diabetes [26]. This finding suggests the existence of a potent additive effect.

According to the ’thrifty phenotype’ hypothesis [27], [28], the combination of being undernourished in utero followed by a nutritionally overabundant environment later in life may unmask certain fetally programmed predispositions such as central adiposity, decreased pancreatic beta-cell growth, sub-normal insulin secretory responses and insulin receptors functions, and activity of the hypothalamic–pituitary–adrenal axis). These abnormalities in turn, may increase susceptibility to insulin resistance and type 2 diabetes [4], [29], [30], [31], [32].

2.5. Large for gestational age 

As the prevalence of obesity has increased among women of childbearing age, so has the number of large for gestational age (LGA) births [33], [34]. Several studies have found that being born LGA is associated with increased risk of type 2 diabetes in adults [35], [36]. However, the analysis is complicated due to the fact that diabetes during pregnancy is a risk factor for being born LGA, and may confer diabetes risk to offspring independent of effects on birth weight. In other words, LGA may simply be a covariate in the relationship between maternal hyperglycemia and type 2 diabetes in offspring.

2.6. Maternal diabetes during pregnancy 

The incidence of diabetes during pregnancy has increased the incidence of pediatric type 2 diabetes [37], [38]. In addition to increasing the risk of LGA in offspring, maternal diabetes during pregnancy is a risk factor for overweight, impaired glucose tolerance, and frank Type 2 diabetes among the offspring [39], [40]. In a longitudinal study, half of the offspring born to mothers with diabetes had weights above the 90th percentile for gestational age at birth, half had BMI's above the 90th percentile by age 8 years, and over a third developed impaired glucose tolerance by adolescence [41], [42].

2.7. Breastfeeding 

Two studies, one if Native Americans and another in Native Canadians, have reported that breastfeeding was associated with protection against subsequent development of type 2 diabetes. In the study of Pima Indians, diabetes was less common among youth (10–19 years of age) who were exclusively breastfed for their first 2 months of life (none of 56 youth had type 2 diabetes) than among youth exclusively bottle-fed (six of 165 youth or 3.5% had type 2 diabetes) [39], [43]. In the study of Native Canadians, breastfeeding longer than 12 months was associated with a reduced rate of type 2 diabetes among youth, independent of BMI [44].

2.8. Summary of the identified risk factors 

Overweight is the most critical risk factor, and should be targeted for prevention of type 2 diabetes especially among youths. Diet and physical activity, which mediate energy balance, are also clearly related to diabetes risk. Ethnicity and perinatal factors (i.e., being born either LGA or SGA or to a mother with diabetes during pregnancy) may also be risk factors. The risk appears to be of particular importance for certain ethnic groups. Perinatal factors include non-modifiable and modifiable risk factors for the development of type 2 diabetes, and therefore should be included in the preventive strategies. Non-modifiable risk factors useful in identifying high-risk youths include family history of type 2 diabetes. The interaction of these factors may be schematically presented in the following (Table 1, Table 2, Table 3).

Table 1. Summary of studies involving interventions (no medications)
StudyNumber of peopleYears of follow-upMean age, mean BMIType of interventionFrequency of interventionTargetsEffect of intervention
Malmo, Sweden [52], [53]181 (men only)6.048 years, 26kg/m2Diet, exerciseMonthly for 6/12, then every 12/12Unspecified weight lossReduction in diabetes incidence in intervention group 37% 2.0–3.3kg weight loss
Da Qing, China [54]5776.045 years, 25.6kg/m2Diet, exercise or both7 sessions in 3/12, then every 3/12BMI<23kg/m2, healthier dietReduction in diabetes incidence per group: 31%
DPS, Finland [55]5223.255 years, 31kg/m2Diet, exercise7 sessions in 12/12, then every 3/12. Free gym membershipand supervised activitysessions5% weight loss, decrease fat intake, increase fibre intake >150min exercise/weekReduction in diabetes incidence in intervention group—58% (63% in men and 54% in women) 3.5kg weight loss after 2 years
New Zealand [56]1035.052 years, 29kg/m2DietMonthly for first 12/12Unspecified weight loss, reduced fat intakeNo benefit in progression to diabetes. No weight loss
Malmohus, Sweden [57]267 (men only)10.054.1 years (mean weight 76kg)Diet, exerciseEvery 12/12 Reduction in diabetes—13% diet group, 29% control, no weight loss
FHS [58]1886.050 years (mean weight 81.7kg)Diet, exerciseEvery 3/12Lose weight if BMI>22kg/m2, low fat diet, exercise 3–4 times/weekNo benefit in progression to diabetes. No weight loss
DPP, US [59]32342.851 years, 34kg/m2Diet, exercise16 diet sessions in 6/12, then monthly. Twice weekly supervised exercise sessions7% weight loss, low-fat diet, 150min exercise/weekDecreased progression to diabetes per group 58% diet and exercise. 3.8kg weight loss

Indian Diabetes Prevention Programme (IDPP) [51]5313.045.9 years, 25.8kg/m2Diet and exercise metfromin; diet, exercise and metformin6 months interval• Unspecified weight lossReduction in diabetes incidence in: LSM −28.5%; Met Group −26.4%; LSM+Met −28.2%
• Reduce calorie and fat intake
• Moderate physical activity
Table 2. Summary of studies involving lifestyle interventions with oral Hypoglycaemic agents
StudyNumber of peopleInclusion criteriaYears of fol-low upMean age, mean BMIOral hypoglycaemic agentType of interventionFrequency of interventionSpecified targets other than to delay progression to diabetesEffect of intervention
Malmohus, Sweden [60]267 (men only)IGT using a 30g glucose/m2 body surface area OGTT: 1hglucose>8.9, 2hglucose>6.7; 3hglucose>4.7mmol/l1054.1 years (mean weight 76kg)TolbutamideDiet, exercise, weight lossEvery 12/12–Decreased progression to diabetes per group; 29%. No weight loss
Whitehall [61]2002h glucose value after 50g OGTT 6.7–11.0mmol/l556 years, 26.2kg/m2PhenforminCarbohydrate restricted dietOnce at start of studyUnspecified weight lossNo benefit in progression to diabetes, weight loss 1.2kg
FHS [62]188Fasting glucose 5.5–7.7mmol/l650 years (mean weight 81.7kg)GliclazideDiet, exerciseEvery 3/12Lose weight if BMI>22kg/m2, low fat diet, exercise 3–4times/weekNo benefit in progression to diabetes, no weight loss
DPP, US [59], [63], [64]3234IGT+fasting glucose >5.3mmol/l. 45% ethnic minority2.851 years, 34kg/m2MetforminDiet, exercise16 diet sessions in 6/12, then monthly. Twice weekly supervised exercise sessions7% weight loss, low-fat diet, 150min exercise/weekDecreased progression to diabetes per group; 58% diet and exercise (71% in people aged >70) ”>metformin. 3.8kg weight loss diet+exercise. 1.8kg weight loss metformin
STOP NIDDM [65], [66]1429IGT+fasting glucose >5.6mmol/l3.355 years, 31kg/m2AcarboseGeneral advice on diet, weight loss and activity.Every 12/12–Acarbose decreased progression to diabetes by 25%. Weight loss 0.5kg
EDIT [67], [68]631Fasting glucose 5.5–7.7mmol/l652 years, 28.6kg/m2Metformin, acarbose or bothNoneUnspecified–In patients with IGT at baseline, decreased risk of progression to diabetes with acarbose, no weight loss
IDPP [51]531Fasting glucose <7.0mmol/l; 2h glucose 7.8–11.0mmol/l345.9 years, 25.8kg/m2MetforminDiet and exercise metformin; Diet, exercise and metformin6 months intervalUnspecified weight loss; reduce calorie and fat intake; moderate physical activityReduction in diabetes incidence in: LSM −28.5%; Met −26.4%; LSM+Met −28.2%
Table 3. Summary of downstream interventions
StudyCumulative incidence of Type 2DM vs. placebo (%).InterventionNumber needed to treatDuration (years)
Indian Diabetes Prevention Programme (IDPP) [51]55 vs. 39.3Lifestyle6.43
Da Qing [54]66 vs. 44Lifestyle4.56
DPS, Finland [55]42 vs. 32Lifestyle84
DPP [59], [63], [65]29 vs. 14Lifestyle73
DPP [59], [63], [64]29 vs. 22Metformin143
STOP–NIDDM [65]42 vs. 32Acarbose114
TRIPOD [69]30 vs. 14Troglitazone62.5
XENDOS [70]9 vs. 6Xenical363

Indian Diabetes Prevention Programme (IDPP) [51]55 vs. 40.5Metformin6.93
55 vs. 39.5LSM+Met6.53

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3. Primary prevention 

Primary prevention can be defined as the prevention of a disease by targeting or controlling modifiable risk factors in a population [45]. In broad terms, prevention programmes have been described as downstream, midstream or upstream [46].

Downstream programmes are where individuals at the highest risk are targeted. Midstream programs target defined populations or communities who are thought to be at an increased risk of diabetes. Upstream programmes include public policy and environmental interventions directed at the entire population to increase support for healthy lifestyle behaviours [46].

The need for preventative strategies for type 2 diabetes is clear [47], [48]. Traditional medical approaches may not be sufficient to avert what has been referred to as a ‘doomsday’ scenario [49]. It has been suggested that major changes in the socio-economic and cultural status of people in developing countries and in disadvantaged minority groups in developed countries are needed in order to make a significant impact [49]. We will briefly look at the modifiable risk factors for type 2 diabetes and evidence for downstream, midstream and upstream programs in terms of progression to diabetes and mortality outcomes.

3.1. Preventive strategies 

On the basis of these modifiable risk factors for type 2 diabetes many of the prevention programs have focussed on lifestyle modifications, although other strategies including the use of pharmacological agents, which target either improvement in the beta-cell function or insulin resistance, have also been used.

In the U.S. Diabetes Prevention Programme (DPP), had three arms in the study, the placebo, metformin and intensive life style changes. After an average follow-up of 2.8 years, there was a 58% relative reduction in the progression to diabetes in the lifestyle group compared with the control group. Within this group, 50% achieved the goal of more than 7% weight reduction, and 74% maintained at least 150min of moderately intense activity each week [50]. It is interesting that the Indian Diabetes Prevention Programme (IDPP) showed that diabetes was significant role of moderate, lifestyle modification (LSM) even without significant weight reduction [51].

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4. Conclusions 

There is a rising need among the professionals and policy makers to focus on prevention of type 2 diabetes. Upstream interventions have the potential for making the largest impact on diabetes. However, it is unlikely that a study would ever be undertaken to demonstrate an impact of upstream intervention on the incidence of diabetes or cardiovascular outcomes. It is difficult in the sense of logistics, economy and ethical dilemma in replicating randomised controlled trials in the general population over a prolonged period of time. The most beneficial population-based measures are increased physical activity and decreased consumption of energy-dense foods. This needs combined efforts from governments and research to make the necessary sustainable changes in food consumption and education policy, models of which has been shown to work in Finland [14].

Midstream interventions need to be developed further and evaluated, particularly those that target school children and young people. Other interventions involving ethnic groups, women with gestational diabetes and obese subjects appear to be promising.

The clearest evidence of benefit is in downstream interventions. Targeting those patients with IGT with lifestyle and interventions focused around increasing activity and altering dietary factors has been particularly effective in North American and Finnish populations. Similar results have been obtained in the Asian Indians in a primary prevention study in subjects with IGT. The trials that have produced significant results targeted people at high risk of diabetes, had intensive on-going interventions and were organized and coordinated by people committed to achieving results. This may suggest that same strategies may fail to produce the same results, as differing social, economic, political and cultural environments will affect diet and lifestyle.

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Competing interests 

The authors declare that they have no competing interests.

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Author's contribution 

All the authors have contributed in all the tasks, while the first author took the responsibility for the over all presentation and the writing

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Acknowledgement 

We like to acknowledge all the members of the network ImmiDiab for their contributions and hard work to the project.

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PII: S0168-8227(06)00426-8

doi:10.1016/j.diabres.2006.09.020

Diabetes Research and Clinical Practice
Volume 76, Issue 3 , Pages 317-326, June 2007

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