SECTION 1

Background

Chapter 1.1

Prevalence, public health aspects and prevention of diabetes

Pamela Dyson

University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK

1.1.1 Prevalence

Globally, diabetes is one of the most common non-communicable diseases (NCD), affecting an estimated 371 million people (8.3% of the adult population) worldwide in 2012 [1]. Type 2 diabetes accounts for 85–90% of global diabetes, and conservative estimates by the International Diabetes Federation (IDF) predict that diabetes will increase to 776 million by 2035 (9% of the population), and that over 80% of those with diabetes will live in low and middle-income countries (LMIC) [2]. The predicted increase in diabetes is largely due to type 2 diabetes and is strongly associated with lifestyle factors, including obesity, physical inactivity and unhealthy diet. The rising incidence of diabetes is not confined to one part of the world and the IDF reports a wide geographic spread. Table 1.1.1 shows the rising pandemic, split by world region. It illustrates that the diabetes epidemic, although well established in high-income countries, will be much more prominent as an increasing problem in LMIC. For example, it is predicted that the number of people with diabetes will double in Africa and the Middle East and North Africa between 2010 and 2030.

Table 1.1.1 Regional estimates for diabetes (20–79 age group), 2010 and 2030

Key: NAC North America and Caribbean, MENA Middle East and North Africa, SEA South East Asia, EUR Europe, SACA South and Central America, WP Western Pacific, AFR Africa

Source: Diabetes Atlas 6th edition.

Approximately 80–90% of those with diagnosed diabetes have type 2 diabetes and 10–20% have type 1 diabetes. Different countries exhibit different rates of diabetes with a range from <5% in parts of Africa to >30% amongst adults in Narau. In the United Kingdom (UK), prevalence rates were estimated at 4.26% (2.8 million adults) in 2010 based upon data from the Qualities and Outcomes Framework [3] although this may be an underestimate as a more recent study reported that the prevalence amongst adults in the UK was 3.1 million (7.4%) in 2011 [4].

The global statistics for the prevalence of diabetes refer only to those who have received a diagnosis but population-based studies have reported a high prevalence of undiagnosed diabetes. Globally, approximately 175 million people may be unaware of their diabetes [2] and in the UK, for example, it has been estimated that 850 000 people are living with undiagnosed diabetes [5]. There are large differences between countries for the prevalence of undiagnosed diabetes, with rates of 90% reported in some African countries and much lower rates in high-income countries. As with diagnosed diabetes, over 80% of people with undiagnosed diabetes live in LMIC.

1.1.2 Pre-diabetes

Pre-diabetes or impaired glucose tolerance (IGT) is characterized by elevated blood glucose levels, and is considered a risk factor for the development of type 2 diabetes and for cardiovascular disease. Approximately 316 million people in the world were estimated to have IGT in 2013, and 70% of these live in LMIC. By 2035, the numbers with IGT are projected to increase to 471 million, meaning that over one billion people, or approximately 20% of the adult population, will be living with diabetes or pre-diabetes by 2035 [2].

1.1.3 Public health aspects

Diabetes, in common with other NCDs, is regarded as a clinical disease and is traditionally managed by application of the acute medical model to the individual with diabetes. As type 2 diabetes prevalence has increased, it has become a public health concern requiring a broad, multidisciplinary approach that targets individuals, families, communities and societies. Diabetes requires more than the traditional approach of medical management of each individual, and effective treatment and prevention will entail a population-based public health approach.

Public health includes the concepts of surveillance for assessment and monitoring, prevention strategies and policy implications. Surveillance can provide data about the prevalence of diabetes and associated risk factors, including health behaviour and obesity. These data can be used to define and ultimately reduce the burden of diabetes by targeting services and prevention strategies at relevant populations. Many countries do not maintain national diabetes registers and do not have systems to assess risk factors, and uncertainties about prevalence in the general population and in high-risk groups prevent instigation of effective public heath strategies to prevent and manage diabetes.

Public policies for prevention and management of diabetes can be introduced at local, state and national levels. Management of diabetes can be improved by policies at a national level e.g. the UK retinal screening programme and at a local level e.g. school policies for the management of children with type 1 diabetes. Health care policies are an important factor for the management of diabetes, and integration of health care (whether provided by the state or through private insurance) with public policy is essential.

Economic impact of diabetes

Diabetes affects quality of life, general health and well-being and is responsible for the loss of healthy years of life (disability-adjusted life years or DALYs). The premature mortality associated with diabetes is preceded by years of disability. Apart from the human consequences of the morbidity and mortality associated with diabetes, the economic impact is enormous and is related to both the direct medical costs of treatment and the indirect costs of labour units lost. Type 2 diabetes in particular is now affecting people at a younger age during their prime economically productive years and it has been estimated that the global economic impact could total US $490 billion over the next 20 years [2]. The estimated global cost of diabetes alone was US $471 billion in 2012, accounting for 11–12% of total healthcare expenditure in the world. Diabetes is forecast to have substantial negative effects on individual, national and international economic well-being over the next 20 years, and this will have particular effect in newly emerging economies.

1.1.4 Prevention

Type 1 diabetes

The aetiology of type 1 diabetes remains poorly understood and there is no evidence for effective prevention; studies in high-risk groups have used strategies including insulin therapy [6] and nicotinamide supplementation [7] without success. A more recent randomised controlled trial is investigating early exposure to complex dietary proteins in high-risk infants and has shown a reduction of approximately 50% in diabetes-associated antibodies in those weaned to a highly hydrolysed formula. Whether this translates to diabetes prevention will be clear at the study’s end in 2017 [8].

Type 2 diabetes

Risk factors for type 2 diabetes include both non-modifiable (age, genetic predisposition, ethnicity) and modifiable (obesity, physical inactivity, diet) factors. There is strong evidence for type 2 diabetes prevention from studies in high-risk individuals from different ethnic groups, using both pharmacological and lifestyle interventions [9–13]. The most effective intervention is that of lifestyle change, incorporating weight loss, dietary modification and increased physical activity; this combination can reduce the risk of diabetes by 28–59% [14,15]. In addition, three studies have reported long-term reductions in progression to diabetes in lifestyle intervention groups at 7–20 years after completion of the study – the so-called legacy effect [16–18].

Components of lifestyle interventions

The main components of lifestyle interventions for diabetes prevention were similar in all published studies. The Diabetes Prevention Programme (DPP) achieved 7% weight loss amongst participants by recommending an energy deficit of 500–1000 kcal/day, reduction of fat intake to 25% total energy intake and promoting 150 minutes of moderate activity per week [9]. The Finnish Diabetes Prevention Study (DPS) recommended ≥5% weight loss, a reduction in total fat intake to <30% and saturated fat to <10% total energy, an increase in fibre intake to ≥15 g/1000 kcal and 30 minutes of moderate physical activity daily [10]. The Indian diabetes prevention study included energy restriction, fat reduction, avoidance of sugar and increased dietary fibre. In addition, participants were asked to take > 30 minutes of moderate exercise daily [11]. The Japanese prevention trial promoted weight loss by a 10% reduction in portion size for all foods except vegetables, low fat intake (<50 g/day) and low alcohol intake (<50 g/day) with 30–40 minutes of moderate exercise per day [12]. The Chinese study attempted to define the relative effects of physical activity, diet and a combination of the two by adopting block randomisation, although specific details of each intervention are not described [13].

Weight loss

The most dominant predictor for diabetes prevention is weight loss; every kilogram lost is associated with a 16% reduction in risk [14]. Although all the published data support the use of a low fat, increased fibre, moderate energy reduction diet, there are no head to head trials assessing the most effective strategy for weight loss and diabetes prevention [19]. There is limited evidence that alternative approaches, including the Mediterranean diet [20], meal replacements [21] and low carbohydrate diets [22] may be effective for weight loss and diabetes prevention in high-risk individuals.

Dietary components

Epidemiological studies have shown that specific foods may have a role in diabetes prevention, including higher intakes of low fat dairy products [23,24] dark yellow [25] and green leafy vegetables [26] and coffee [27]. Moderate intakes of alcohol also protect against diabetes [28]. Some foods are associated with a higher risk of diabetes and these include red and processed meat [29] and fried potato products [30].

In addition, there are also specific vitamins and minerals that have been associated with a lower incidence of diabetes, although these are usually taken as supplements rather than obtained from food. Epidemiological evidence suggests that high intakes of Vitamin D and calcium [31] and magnesium [32] may reduce risk, but the effect of chromium remains uncertain[ 33].

Physical activity

Increased physical activity reduces the risk of diabetes, and at least 30 minutes per day of moderate activity has been recommended by most studies.

Guidelines for diabetes prevention

European evidence-based guidelines for diabetes prevention have recently been published [34], and the American Diabetes Association and Diabetes UK have included lifestyle-specific guidelines in their latest recommendations for the prevention and management of diabetes [35,36]. These guidelines recommend:

Intensive lifestyle interventions incorporating low fat, high fibre diets and increased physical activity should be used to prevent diabetes in adults.

Weight reduction is an essential component of prevention, and long-term losses of 5–7% are effective.

At least 30 minutes of moderate physical activity should be taken daily.

One of the most challenging aspects of diabetes prevention remains the application of positive results from clinical trials into routine clinical use. There are on-going studies investigating different strategies in the community [37–39] but at present these trials are aimed at high-risk individuals [40] and there is little evidence of translation of the success of randomised controlled trials to public health and, as a result, global diabetes prevalence continues to rise.

Key points

Diabetes affected 8.3% of the global adult population in 2013, with 80% of those living in low / middle income countries.

Significant numbers are either undiagnosed or have pre-diabetes.

Prevalence of type 2 diabetes is increasing due to ageing, physical inactivity and increasing obesity.

There is no evidence for prevention of type 1 diabetes.

There is strong evidence for the role of lifestyle in the prevention of type 2 diabetes in high-risk individuals.

A healthy lifestyle, including weight loss and increased physical activity, is the cornerstone of diabetes prevention.

References

1. WHO. World Health Statistics 2012. Geneva: World Health Organization, 2012.

2. International Diabetes Federation. Diabetes Atlas, 6th edn, Brusssels, Belgium: International Diabetes Federation, 2013.

3. NHS. Quality and Outcomes Framework. Online GP practice results database, 2010.

4. Holman N, Forouhi NG, Goyder E, Wild SH. The Association of Public Health Observatories (APHO) Diabetes Prevalence Model: estimates of total diabetes prevalence for England, 2010–2030. Diabet Med 2011; 28(5): 575–82.

5. Diabetes UK. State of the Nation: England 2012. London: Diabetes UK, 2012.

6. Diabetes Prevention Trial - Type 1 Diabetes Study Group. Effects of insulin in relatives of people with type 1 diabetes mellitus. N Eng J Med 2002; 346: 1685–1691.

7. Gale EA, Bingley PJ, Emmett CL, Collier T; European Nicotinamide Diabetes Intervention Trial (ENDIT) Group. European Nicotinamide Diabetes Intervention Trial (ENDIT): a randomised controlled trial of intervention before the onset of type 1 diabetes. Lancet 2004; 363(9413): 925–931.

8. Knip M, Virtanen SM, Becker D, Dupré J, Krischer JP, Akerblom HK; for the TRIGR Study Group. Early feeding and risk of type 1 diabetes mellitus: experiences from the Trial to Reduce Insulin-dependent diabetes Mellitus in the Genetically at Risk (TRIGR). Am J Clin Nutr 2011: 94(Suppl 6): 1814S–1820S.

9. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, et al.; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346(6): 393–403.

10. Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, et al.; Finnish Diabetes Prevention Study Group. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001; 344(18): 1343–1350.

11. Ramachandran A, Snehalatha C, Mary S, Mukesh B, Bhaskar AD, Vijay V; Indian Diabetes Prevention Programme (IDPP). The Indian Diabetes Prevention Programme shows that lifestyle modification and metformin prevent type 2 diabetes in Asian Indian subjects with impaired glucose tolerance (IDPP-1). Diabetologia 2006; 49(2): 289–297.

12. Kosaka K, Noda M, Kuzuya T. Prevention of type 2 diabetes by lifestyle intervention: a Japanese trial in IGT males. Diabetes Res Clin Pract 2005; 67: 152–162.

13. Pan XR, Li GW, Hu YH, Wang JX, Yang WY, An ZX, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20(4): 537–544.

14. Walker KZ, O'Dea K, Gomez M, Girgis S, Colagiuri R. Diet and exercise in the prevention of diabetes. J Hum Nutr Diet 2010; 23(4): 344–352.

15. Knowler WC, Fowler SE, Hamman RF, Christophi CA, Hoffman HJ, Brenneman AT, et al.; Diabetes Prevention Programme Research Group. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet 2009; 374(9702): 1677–1686.

16. Li G, Zhang P, Wang J, Gregg EW, Yang W, Gong Q, et al. The long-term effect of lifestyle interventions to prevent diabetes in the China Da Qing Diabetes Prevention Study: a 20-year follow-up study. Lancet 2008; 371(9626): 1783–1789.

17. Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, et al.; Finnish Diabetes Prevention Study Group. Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 2006; 368(9548): 1673–1679.

18. Diabetes Prevention Programme (DPP) research group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care 2002; 25(12): 2165–2171.

19. Hamman RF, Wing RR, Edelstein SL, Lachin JM, Bray GA, Delahanty L, et al. Effect of weight loss with lifestyle intervention on risk of diabetes. Diabetes Care 2006; 29(9): 2102–2107.

20. Salas-Salvadó J, Martinez-González MA, Bulló M, Ros E. The role of diet in the prevention of type 2 diabetes. Nutr Metab Cardiovasc Dis 2011; 21(Suppl 2): B32–48.

21. Noakes M, Foster PR, Keogh JB, Clifton PM. Meal replacements are as effective as structured weight-loss diets for treating obesity in adults with features of metabolic syndrome. J Nutr 2004; 134(8): 1894–1899.

22. Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev 2009; 10(1): 36–50.

23. Choi HK, Willett WC, Stampfer MJ, Rimm E, Hu FB. Dairy consumption and risk of type 2 diabetes mellitus in men: a prospective study. Arch Intern Med 2005; 165(9): 997–1003.

24. Liu S, Choi HK, Ford E, Song Y, Klevak A, Buring JE, et al. A prospective study of dairy intake and the risk of type 2 diabetes in women. Diabetes Care 2006; 29(7): 1579–1584.

25. Liu S, Serdula M, Janket SJ, Cook NR, Sesso HD, Willett WC, et al. A prospective study of fruit and vegetable intake and the risk of type 2 diabetes in women. Diabetes Care 2004; 27(12): 2993–2996.

26. Carter P, Gray LJ, Troughton J, Khunti K, Davies MJ. Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis. BMJ 2010; 341: 4229.

27. van Dam RM, Willett WC, Manson JE, Hu FB. Coffee, caffeine, and risk of type 2 diabetes: a prospective cohort study in younger and middle-aged U.S. women. Diabetes Care 2006; 29(2): 398–403.

28. Wannamethee SG, Camargo CA Jr, Manson JE, Willett WC, Rimm EB. Alcohol drinking patterns and risk of type 2 diabetes mellitus among younger women. Arch Intern Med 2003; 163(11): 1329–1336.

29. van Dam RM, Willett WC, Rimm EB, Stampfer MJ, Hu FB. Dietary fat and meat intake in relation to risk of type 2 diabetes in men. Diabetes Care 2002; 25(3): 417–424.

30. Halton TL, Willett WC, Liu S, Manson JE, Stampfer MJ, et al. Potato and french fry consumption and risk of type 2 diabetes in women. Am J Clin Nutr 2006; 83(2): 284–290.

31. Pittas AG, Dawson-Hughes B, Li T, Van Dam RM, Willett WC, Manson JE, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care 2006; 29(3): 650–656.

32. Larsson SC, Wolk A. Magnesium intake and risk of type 2 diabetes: a meta-analysis. J Intern Med 2007; 262(2): 208–214.

33. Trumbo PR, Ellwood KC. Chromium picolinate intake and risk of type 2 diabetes: an evidence-based review by the United States Food and Drug Administration. Nutr Rev 2006; 64(8): 357–363.

34. Paulweber B, Valensi P, Lindström J, Lalic NM, Greaves CJ, McKee M, et al. A European evidence-based guideline for the prevention of Type 2 diabetes. Horm Metab Res 2010; 41(Suppl 1): S3–S36.

35. Evert AB, Boucher JL, Cypress M, Dunbar SA, Franz MJ, Mayer-Davis EJ, et al. Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care 2014 Jan; 37(Suppl 1): S120–S143.

36. Dyson PA, Kelly T, Deakin T, Duncan A, Frost G, Harrison Z, et al.; Diabetes UK Nutrition Working Group. Diabetes UK evidence-based nutrition guidelines for the prevention and management of diabetes. Diabet Med 2011 Nov; 28(11): 1282–1288.

37. Ackermann RT, Marrero DG. Adapting the Diabetes Prevention Program lifestyle intervention for delivery in the community: the YMCA model. Diabetes Educ 2007; 33(1): 69, 74–75, 77–78.

38. Lakerveld J, Bot SD, Chinapaw MJ, van Tulder MW, van Oppen P, Dekker, JM, et al. Primary prevention of diabetes mellitus type 2 and cardiovascular diseases using a cognitive behavior program aimed at lifestyle changes in people at risk: Design of a randomized controlled trial. BMC Endocr Disord 2008; 8: 6.

39. Williams K, Prevost, AT, Griffin S, Haredeman W, Hollingowrth W, Spiegelhalter D, et al. The ProActive trial protocol - a randomised controlled trial of the efficacy of a family-based, domiciliary intervention programme to increase physical activity among individuals at high risk of diabetes [ISRCTN61323766]. BMC Public Health 2004; 4: 48.

40. Uusitupa M, TuomilehtoJ, Puska P. Are we really active in the prevention of obesity and type 2 diabetes at the community level? Nutr Metab Cardiovasc Dis 2011; 21(5): 380–389.

Chapter 1.2

Diagnostic criteria and classification of diabetes

Pamela Dyson

University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK

1.2.1 Diagnostic criteria

Diabetes

The diagnostic criteria for diabetes have been developed and revised by the World Health Organisation (WHO) [1] and use the occurrence of diabetes-specific complications to derive diagnostic cut-points for diabetes. A diagnosis of diabetes can be made under the following circumstances:

fasting plasma glucose > 7.0 mmol/l (126 mg/dl)

or 2-hour glucose > 11.1 mmol/l (200 mg/dl) after ingestion of a 75 g oral glucose load (oral glucose tolerance test – OGTT)

Glycaemia is commonly assessed by a test known as HbA1c, a simple blood test measuring levels of glycated haemoglobin, and both the WHO and American Diabetes Association (ADA) now support its use as a suitable test for the diagnosis of diabetes [2,3]. HbA1c can be used for the diagnosis of diabetes, but only if the assays are standardised to international reference levels and if stringent quality assurance is in place. The cut-off point is 48 mmol/mol (6.5%), although a value <48 mmol/mol does not exclude diabetes if it has been previously diagnosed based upon blood glucose measurements. The advantage of using HbA1c as a diagnostic test is that it uses a non-fasting sample and does not require the dietary preparation necessary for an OGTT. The disadvantages of HbA1c are that it is relatively expensive, not widely available in low and middle-income countries (LMIC) and the result may be affected by a variety of factors including haemoglobinopathies. In addition, the WHO states that a diagnosis of diabetes should not be made based upon a single abnormal HbA1c value in the absence of symptoms, and that at least one additional test of HbA1c, or plasma glucose levels (fasting or 2-hour following OGTT) should be taken to confirm the diagnosis.

Impaired glucose tolerance and increased fasting glucose

Both impaired glucose tolerance (IGT) and increased fasting glucose (IFG) have been identified as risk factors for developing diabetes, and IGT as a risk factor for cardiovascular disease. The diagnostic criteria for IGT and IFG are:

Impaired Glucose Tolerance: fasting plasma glucose < 7.0 mmol/l (126 mg/dl) and 2-hour plasma glucose > 7.8 and <11.1 mmol/l (140 and 200 mg/dl) after OGTT

Increased Fasting Glucose: fasting plasma glucose 6.1 – 6.9 mmol/l (110 – 125 mg/dl) and (if measured) 2-hour glucose < 7.8 mmol/l (142 mg/dl)

Gestational diabetes

There is no agreed international standard for the screening and diagnosis of gestational diabetes (GDM), although there is consensus that the diagnosis of diabetes during pregnancy should use similar criteria to those for adults generally [4,5]. A more recent report has caused some controversy by recommending changes to the diagnosis of GDM and advocating screening for women with risk factors in early pregnancy, with screening for all other women at 24–28 weeks of pregnancy [6]. A 75 g OGTT is recommended as the test for GDM and a diagnosis should be made if any one glucose level reaches a specified level of:

Fasting > 5.1 mmol/l

1-hour > 10.0 mmol/l

2-hour > 8.5 mmol/l

There is concern that these new diagnostic criteria will increase the diagnosis of GDM and will have a large impact on resources without proven benefit [7].

1.2.2 Classification

There are two broad categories of diabetes: type 1 and type 2, although other rarer categories do exist.

Type 1 diabetes

Type 1 diabetes is an autoimmune condition characterised by pancreatic β-cell failure leading to complete insulin deficiency and susceptibility to ketoacidosis. It is usually characterised by the presence of anti-GAD, islet cell or insulin antibodies, although these may not be present in certain cases and this type of diabetes is referred to as ‘idiopathic type 1’. The cause of type 1 diabetes remains unknown, although genetic factors and certain viruses may play a part. Type 1 diabetes usually presents in children and young adults, although it can be diagnosed at any age. Type 1 diabetes accounts for approximately 10–20% of diabetes and is treated by a combination of insulin replacement by injection or pump therapy and lifestyle modification.

Type 2 diabetes

Type 2 diabetes is characterised by defects in insulin secretion, usually accompanied by resistance to the action of insulin. Type 2 diabetes accounts for 80–90% of diabetes and has a strong genetic propensity to run in families, but is also associated with lifestyle factors and is more common in societies with high levels of obesity and low levels of physical activity. The risk factors for type 2 diabetes include non-modifiable (age, race and genetic predisposition) and modifiable (obesity, physical inactivity and unhealthy diet). Approximately 80–90% of people with type 2 diabetes are overweight or obese, and a recent European study has shown that nearly 50% of people with diabetes are obese (BMI >30 kg/m²), twice the prevalence in the background population [8]. It is most frequently diagnosed in the middle-aged and elderly population, typically in people over the age of 40, although it is now increasingly diagnosed in obese children and adolescents. Traditionally, over 95% of diabetes in children is categorised as type 1, but in the United States (US), among older children, the proportion of type 2 diabetes ranges from 6% in non-hispanic white adolescents to 76% in American Indians [9]. Despite reports from around the world of an increase in the incidence of type 2 diabetes in children and adolescents, the true prevalence is largely unknown, although it is estimated that the prevalence in the United States (US) is approximately 12 per 100 000 [10]. The majority of type 2 diabetes is found in ethnic groups, including African-Americans, Hispanic, Pacific Islanders, with the highest prevalence reported in Pima Indian adolescents (22.3 per 1000) [11]. It has been estimated that as many as 1400 children in the United Kingdom (UK) had type 2 diabetes [12] in 2004, but recent evidence based on prescription of anti-diabetic medication suggests that the prevalence may be as high as 1.9 per 100 000 [13]. Type 2 diabetes is treated by a combination of diet, physical activity, oral medications and, increasingly, injectable therapies, including GLP-1 agonists and insulin.

Other types of diabetes

Genetic defects in β-cell function (maturity onset diabetes in the young – MODY)

Genetic defects in insulin action

Diseases of the exocrine pancreas, including cancer, acute and chronic pancreatitis, cystic fibrosis

Drug-induced diabetes e.g. glucocorticoids, thyroid hormone, thiazide diuretics.

Key points

Diabetes can be diagnosed by three different means; fasting glucose, 2-hour glucose after an oral glucose tolerance test or HbA1c levels.

IFG and IGT are risk factors for type 2 diabetes.

There is no consensus for the diagnosis of gestational diabetes.

There are two main types of diabetes; type 1 and type 2.

References

1. World Health Organization. Definition and diagnosis of diabetes mellitus and intermediate hyperglycaemia: Report of a WHO/IDF consultation. Geneva: World Health Organization, 2006.

2. International Expert Committee. International Expert Committee report on the role of A1c assay in the diagnosis of diabetes. Diabetes Care 2009; 32: 1327–1334.

3. World Health Organization. Use of glycated haemoglobin (HbA1c) in the diagnosis of diabetes mellitus. Geneva: World Health Organization, 2011.

4. WHO Expert Committee on diabetes mellitus: Second report. Geneva: World Health Organization, 1980.

5. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2009; 32(Suppl 1): S62–S67.

6. Metzger BE, Gabbe SG, Persson B, Buchanan TA, Catalano PA, Damn P, et al. International association of diabetes and pregnancy study group recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010; 33(3): 676–682.

7. Cundy T. Proposed new diagnostic criteria for gestational diabetes – a pause for thought? Diabet Med 2011; 29(2): 176–180.

8. Haslam DW. UK findings on overweight, obesity and weight gain from PANORAMA, a pan-European cross-sectional study of patients with Type 2 diabetes. Diabet Med 2011; 28(Suppl 1): 264–265.

9. Liese AD, D’Agostino RB, Hamman RF, Filgo PD, Lawrence JM, Liu LI, et al. The burden of diabetes mellitus among US youth: prevalence estimates from the SEARCH for Diabetes in Youth Study. Pediatrics 2006; 118(4): 1510–1518.

10. Reinehr T. Type 2 diabetes mellitus in children and adolescents. World J Diabetes 2013; 4(6): 270–281.

11. Fagot-Campagna A, Pettitt DJ, Engelgau MM, Burrows NR, Geiss LS, Valdez R, et al. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr 2000; 136: 664–672.

12. Lobstein T, Leach R. Diabetes may be undetected in many children in the UK. BMJ 2004; 328(7450): 1261–1262.

13. Hsia Y, Neubert AC, Rani F, Viner RM, Hindmarsh PC, Wong IC. An increase in the prevalence of type 1 and 2 diabetes in children and adolescents: results from prescription data from a UK general practice database. Br J Clin Pharmacol 2009; 67(2): 242–249.

SECTION 2

Dietary principles of diabetes

Chapter 2.1

Historical perspectives of dietary recommendations for diabetes

Maeve Gacquin

Galway Clinic, Doughiska, Ireland

The nutritional management of diabetes has been subject to much change over the years due to factors such as economic forces, changes in staple foods and eating patterns, new medications and insulin formulations (Table 2.1.1). Since the first published guidelines by the British Diabetic Association in 1982 [1], the availability of evidence-based research and knowledge in science and medicine has improved greatly. This evolution is likely to continue and nutritional recommendations in the future may once again be substantially different from those of today.

Table 2.1.1 Historical changes in the nutritional management of diabetes (Sanders, 2001 [4]; Canadian Diabetic Association, 2008 ADA, 2008 [16]; Diabetes UK, 2011 [18]; Tattersall, 2009 [2])

2.1.1 From early times to the seventeenthth century

In 1000 BC traditional Indian medicine noted two types of diabetes. One that occurred in thin young individuals and one that was common in the overweight [2].

The earliest known record of diabetes was mentioned in a Third Dynasty Egyptian papyrus in 1552 BC by the physician Hesy-Ra and describes polyuria as a symptom [2,3].

The Greeks were the first to advocate diet and lifestyle management. In the first century AD, diabetes was described by Arateus as the ‘melting down of flesh and limbs into urine’. He gave it the name diabetes which means ‘siphon’. Aetius prescribed a ‘cooling diet of diluted wine and cooling applications to the loins’. Avicenna directed that all diuretic foods and drugs be avoided and that patients engage in exercise (preferably on horseback). In the later stages of diabetes he recommended ‘tepid baths and fragrant wines’ [2–4].

In the seventeenthth century a London Physician, Dr Thomas Willis, used urine sampling/tasting to diagnose diabetes ‘mellitus’ (Latin for honey). This method of monitoring remained unchanged till the twentieth century [2–4].

2.1.2 Eighteenth and nineteenth centuries

There were many significant developments in the nineteenth century with key individuals contributing to the understanding and management of diabetes, often with some unusual and unconventional diet and lifestyle measures.

John Rollo, an army surgeon, was interested in the physiology and source of glycosuria. He proposed that sugar may be formed in the stomach from fruit and vegetables and recommended that a diet consisting predominantly of animal foods was appropriate [2–4]. An example of a daily regimen from his 1797 book consisted of:

Breakfast: 1½ pints of milk and a half a pint of lime water mixed together, bread and butter.

Lunch: Plain blood puddings, made of blood and suet only.

Dinner: Game or old meats which have been long kept, and as far as the stomach may bear, fat and rancid old meats.

This type of diet provides 600 kcal a day from carbohydrate and approximately 1200 kcal from fat.

The importance of Rollo’s diet, although seemingly unfavourable for cardiovascular health, was that it was an attempt to treat diabetes rationally by preventing the formation of glucose.

When Dr John Camplin developed the symptoms of diabetes in 1844, he was advised by his colleagues William Prout (1785–1850) and Henry Bence Jones (1814–1873) to adopt a high protein and fat diet [2–4] and, on complaining of ‘great biliary derangement’ and irregular bowel function, Prout introduced him to bran cake. It was also common for physicians of that time to prescribe generous amounts of purgatives such as rhubarb, aloes, senna, magnesium sulfate and castor oil with these high protein, low carbohydrate diets.

One diet that was made popular for a short period by a French physician, Dr Pierre Priory (1794–1879) in the 1850s was sugar feeding [2–4]. His concern was for the amount of sugar lost through urine and he felt that replacing this sugar from dietary sources may restore strength.

In 1870, during the siege of Paris in the Franco-Prussian war, French physician Bourchardat (1806–1886) noticed that, as a result of starvation, the urine of some of his patients was sugar free. Furthermore, incidence rates and mortality rates of type 2 diabetes were shown to decrease during all wars. Bourcardat subsequently advised ‘mangez le moins possible’ (eat as little as possible). Italian Born physician Guelpa (1850–1930) showed that fasting and saline enemas made people with diabetes ‘sugar free’ in three days [2–4].

One feature that has changed very little over the years is that of dietary adherence. At this time many physicians complained of the lack of patient compliance with dietary advice stating that many patients either could not or would not follow the diet. Some ensured dietary compliance with extreme measures. The Italian physician, Catoni kept his patients under lock and key to ensure adherence. Many with diabetes longed for a drug to replace restrictive diets [2].

2.1.3 Twentieth century

By the beginning of the twentieth century many physicians promoted ‘dietary cures’ based on specific foods. These included Donkins skim-milk (1784), Mosse’s potato (1902) and Von Noordens oatmeal cure (1903). The oatmeal diet, for example, consisted of 8 oz of oatmeal and 8 oz of butter daily. These diets included periods of semi-starvation before the introduction of the specific ‘curative’ food [2–4].

During the twentieth century onwards, great emphasis was placed on patient education and diet as the key elements in controlling diabetes. Classes were popular in the United States (US) and Germany while one-to-one education was more common in the United Kingdom (UK). Although well meaning, the teachers had not been taught how to teach and many lesson plans were described as overly scientific and negative or dictatorial.

The author of a 1920 article about diabetes education commented: there is no use talking in the language of the laboratory to a patient that understands only the language of the kitchen. We must either teach them the new language or translate our Greek into understandable English [2]. Unfortunately, this advice was ignored in most diabetes units for the next 60 years and compliance and understanding of diet and lifestyle management of diabetes remained poor.

In 1919 Frederick Allen, a US diabetes physician, published ‘The total regulation of diabetes’. This publication advised the combination of starvation diets with bed rest, often allowing only 450 kcal a day. Although he had some limited success with this approach, many people died of ketoacidosis or undernutrition related illnesses.

The discovery of insulin in 1921 extended the lives of those who were able to obtain a supply, but had little immediate effect on dietary prescriptions. In 1923, for example, the diet remained extremely restrictive; essentially a low carbohydrate intake meant a lower dose of insulin. At the end of the 1920s, some physicians in America and Canada introduced higher carbohydrate diets with the rationale that this type of diet was more palatable, less expensive, achieved greater compliance and, contrary to general expectations, led to a reduction in insulin requirements in many with diabetes. However, many physicians continued to advise low carbohydrate diets due to an ingrained belief that carbohydrate was bad for those with diabetes [2,4].

In 1923, R.D. Lawrence was appointed chief biochemist in King’s College Hospital London. He had been diagnosed with diabetes in 1920 at the age of 28 and developed a strong interest in the management of diabetes. He set up a ‘diet kitchen' where patients could be taught as out-patients about management of diabetes, including diet and insulin injections. He believed ardently that people with diabetes should be given the opportunity to take control of their own treatment and that this would also improve their quality of life. This was predominantly focused at managing type 1 diabetes.

To aid this he devised several influential diet schemes, such as the Line-Ration Diet, now called the Lawrence Weighed diet, and the Lawrence Unweighed Diabetic Diet, providing simple, accurate methods of measuring and regulating dietary intake.

In deriving his diet schemes he aimed to fulfil three main criteria; that each diet should:

Contain sufficient carbohydrate to prevent ketosis.

Satisfy the patient in quantity and quality as far as possible.

Be accurate, simple to calculate, and varied.

In 1925 he published the first edition of ‘The Diabetic Life' and in 1929 he published the first edition of ‘The Diabetic ABC', which he described as a short practical book for patients and nurses. The Lawrence line diet of 1929 aimed to restrict carbohydrate and provide similar amounts of protein, fat and carbohydrate from day to day to ensure consistency. Carbohydrates were labelled as ‘black lines’ and protein and fat were labelled as ‘red lines’. Each black line provided 10g carbohydrate and 40 kcal and each red line provided 111 kcal and 9 g fat. In 1934, Lawrence, with the author H.G. Wells who also had type 1 diabetes, co-founded the Diabetic Association which became known as the British Diabetic Association and is now known as Diabetes UK.

The introduction of the ‘free diets’ during the 1930s caused acrimony and controversy for nearly 30 years. Some physicians believed that a rigid diet in children with diabetes was harmful to mental development and social adjustment, while others maintained a strict low carbohydrate diet [2–4].

2.1.4 Dietary management of type 2 diabetes

The link between obesity and type 2 diabetes was well observed in the twentieth century and outlined as early as 1919 in Frederick Allen’s book ‘The total regulation of diabetes’ but not fully understood. The importance of weight management in type 2 diabetes was demonstrated by landmark studies, such as the UKPDS [5], which demonstrated the direct benefit of moderate weight reduction on improved metabolic control of blood sugar, blood pressure and cholesterol and led to published guidelines for weight management [6].

2.1.5 Carbohydrate counting and exchanges

In the 1960s carbohydrate counting and exchanges were developed by the American Diabetes Association (ADA) for people with diabetes, to help to control blood glucose levels. The carbohydrate exchange diet grouped all the carbohydrate-containing foods into one group. A serving of a carbohydrate-based food was called a carbohydrate exchange and contained 15 g carbohydrate. Standard advice recommended three to four carbohydrate exchanges (similar amounts) with each meal when starting the carbohydrate exchange diet. The number of carbohydrate exchanges could be increased or decreased depending on blood glucose levels, medication and activity.

In the early 1990s the Diabetes Control and Complications Trial (DCCT) used carbohydrate counting as one of its education tools in type 1 diabetes [7].

Carbohydrate counting became increasingly popular once the ADA revised dietary recommendations in 1994. Based on growing scientific evidence that sucrose affects blood glucose levels no differently than other carbohydrates, and that no single meal-planning method works for everyone, the new guidelines essentially lifted the ban on sugar-containing foods to focus attention on controlling total carbohydrate intake and individualising meal plans.

Carbohydrate counting was first embraced by individuals with type 1 diabetes on intensive insulin therapy who used an insulin pump or multiple daily insulin injections. Carbohydrate counting helped those who use insulin to tailor their mealtime dose or bolus of insulin to cover the amount of carbohydrate eaten at that meal. This allowed greater diet and lifestyle flexibility and freedom as the individual could vary the insulin doses depending on carbohydrate intake and activity levels.

Structured education programmes on insulin dose adjustment started in Germany in 1983 [8], and this idea was further developed in the UK as the DAFNE programme [9]. A number of similar education programmes have been developed around the world.

2.1.6 Glycaemic index

During the twentieth century it was observed that certain foods had less effect on blood glucose concentrations after eating, and these foods were identified as those high in protein and fat. Carbohydrate foods have the most significant effect on blood glucose concentrations, but even within this group there was great variation on the rate of the glycaemic effect. In 1981, David Jenkins and his team at the University of Toronto came up with an alternative system of classifying carbohydrate. He ranked the glycaemic effect of commonly eaten carbohydrates and compared them with pure glucose which had a score of 100. He called this the glycaemic index [10]. This system is now widely used and endorsed by all major diabetes authorities.

2.1.7 Development of nutritional guidelines for diabetes

The first position statement on diet and diabetes came from the British Diabetic Association (now known as Diabetes UK) in 1982 [1]. The emphasis of these recommendations was on healthy eating principles in line with those for the general population, which liberalised the diet for many individuals with diabetes. An update of these recommendations from the Nutrition Sub-Committee of the British Diabetic Association Professional Advisory Committee 10 years later in 1992 reinforced the high-carbohydrate low-fat diet [11]. These recommendations were followed by recommendations from the European Association for the Study of Diabetes (EASD) and the ADA in 2000 and 2002, respectively [12,13]. In 2003, Diabetes UK published a document entitled ‘The implementation of nutritional advice for individuals with diabetes’ [14] and this consensus-based paper built on the European and American reviews. The paper discussed the practical implementation of dietary advice for individuals with diabetes and described the provision of services needed to support this approach. The EASD guidelines were also updated and published in 2004 [15].

The move away from consensus-based guidelines towards those that were evidence-based began with dietary guidelines from the ADA in 2008 [16]. The Canadian dietary recommendations were updated in 2008 to reflect Health Canada’s revised ‘Eating well with Canada’s food guide’ and included more flexible recommendations on macronutrient distribution [17]. The most recent evidence-based guidelines from Diabetes UK were published in 2011 [18] and those from the ADA in 2013 [19].

2.1.8 Guidelines for low and middle income ountries

The International Diabetes Federation (IDF) developed a global guideline for the management of type 2 diabetes in 2005 [20]. Published national guidelines often come from relatively resource-rich countries, but the IDF guidelines focus on those that may also be relevant in less well resourced countries. The guidelines focus on physical activity in conjunction with nutrition education and are aimed at different groups in society including families, schools, groups and individuals.

2.1.9 Guidelines for children and adolescents

Children and adolescents have had specific guidelines developed for their use, and the third edition of the International Society for Pediatric and Adolescent Diabetes (ISPAD) Consensus Guidelines, now called Clinical Practice Consensus Guidelines, was published in 2009 in conjunction with the IDF [21].

2.1.10 A change in emphasis

The ADA guidelines in 2008 [16] emphasised that nutrition counselling should be tailored to the individual, with encouragement of low GI carbohydrate foods and adequate vitamin and mineral intake. Low carbohydrate and restricted diets were recommended for weight loss in those with type 2 diabetes, but for 1 year only. Specific guidelines were included for physical activity.

The Diabetes UK 2011 guidelines [18] place an emphasis on carbohydrate management and a more flexible approach to weight loss, unlike previous guidelines which were expressed in terms of recommendations for individual nutrient intakes. These guidelines aim to support self-management, promote healthy lifestyles and reduce the risk of type 2 diabetes and the co-morbidities associated with diabetes. They encourage healthy eating and recommend effective strategies for weight management and glycaemic control.

2.1.11 Summary

Over the years, dietary management of diabetes has been subject to personal whim and anecdotal evidence. History has shown that complicated, restrictive diets are challenging, impractical and unsuccessful for the majority of people with diabetes. The development and improvement of evidence-based dietary recommendations have been important in understanding how to optimise metabolic control, but adherence to diet and lifestyle advice still proves challenging for many people with diabetes. It is essential to continue to develop skills and knowledge on how best to facilitate diet and lifestyle education, learning, motivation and support for individuals and groups with diabetes.

Key points

Dietary treatment of diabetes dates from the Ancient Greeks.

The first diets concentrated on severe carbohydrate restriction.

Over the subsequent years, carbohydrate management was promoted, together with more emphasis on dietary management of cardiovascular risk and body weight.

Today, an individualised, evidence-based approach is recommended by most authorities.

References

1. Nutrition sub-committee of the British Diabetic Association. Dietary recommendations for the 1980s. Hum Nutr: Appl Nutr 1987; 36(5): 378–382.

2. Tattersall R. Diabetes, The Biography. Oxford University Press, Oxford, 2009.

3. Blades M, Morgan JB, Dickerson JW. Dietary advice in the management of diabetes mellitus – history and current practice. JR Soc Health 1997; 117(3): 143–150.

4. Sanders LJ. The Philatelic History of Diabetes. Alexandria, VA: ADA, 2001.

5. King P, Peacock I, Donnelly R. The UK prospective diabetes study (UKPDS): clinical and therapeutic implications for type 2 diabetes. Br J Clin Pharmacol 1999; 48(5): 643–688.

6. Campbell L, Rossner S. Management of obesity in patients with type 2 diabetes. Diabet Med 2001; 18: 345–354.

7. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329(14): 977–986.

8. Muhlhauser I, Bruckner I, Berger M, Cheta D, Jorgens V, Ionescu-Tirqoviste C, et al. Evaluation of an intensified insulin treatment and teaching programme as routine management of type 1 (insulin-dependent) diabetes. The Bucharest-Düsseldorf Study. Diabetologia 1987; 30(9): 681–690.

9. DAFNE study group. Training in flexible, intensive insulin management to enable dietary freedom in people with type 1 diabetes: dose adjustment for normal eating (DAFNE) randomised controlled trial. BMJ 2002; 325 (7367): 746.

10. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34(3): 362–366.

11. Nutrition Sub Committee of the British Diabetic Association Professional Advisory Committee. Dietary recommendations for people with diabetes. An update for the 1990s. Diabet Med 1992; 9: 189–202.

12. Diabetes and Nutrition Study Group of the European Association for the Study of Diabetes. Recommendations for the nutritional management of patients with diabetes mellitus. Eur J Clin Nutr 2000; 54: 353–355.

13. Franz MJ, Bantle JP, Beebe CA, Brunzell JD, Chiasson JL, Garg A, et al. Evidence based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2003; 26(Suppl 1): S51–S61.

14. Nutrition sub-committee of the Diabetes Care Advisory Committee of Diabetes UK. The implementation of nutritional advice for people with diabetes. Diabet Med 2003; 20(10): 786–807.

15. Mann JL, De Leeuw I, Hermansen K, Karamanos B, Karlstrom B, Katsilambros N, et al.; Diabetes and Nutrition Study Group (DNSG) of the European Association for the Study of Diabetes (ESAD). Evidence based nutrition approaches to the treatment and prevention of diabetes mellitus. Nutr Metab Cardiovasc Dis 2004; 14: 373–394.

16. Bantle JP, Wylie-Rosett J, Albright AL, Apovian CM, Clarke NG, Franz MJ, et al. Nutrition recommendations and interventions for diabetes: A position statement from The American Diabetes Association. Diabetes Care 2008; 31(Suppl 1): S61–S78.

17. Canadian Diabetes Association. 2008 Clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2008; 32(Suppl 1): 201.

18. Dyson PA, Kelly T, Deakin T, Duncan A, Frost G, Harrison Z, et al.; Diabetes UK Nutrition Working Group. Diabetes UK evidence-based nutrition guidelines for the prevention and management of diabetes. Diabet Med 2011; 28(11): 1282–1288.

19. Evert AB, Boucher JL, Cypress M, Dunbar SA, Franz MJ, Mayer-Davis EJ, et al. Nutrition therapy recommendations for the management of adults with diabetes.