Module 202.1 en_0

Notes de l'éditeur

1. Section 2 will cover the pathophysiology/classification and prevention of diabetes, nutrition, physical activity and clinical monitoring. This introductory module will explain the different types of diabetes and how a diagnosis is made. It also briefly looks at prevention of both type 1 diabetes and type 2 diabetes.
2. Diabetes (also known as diabetes mellitus) is a group of metabolic diseases, each characterised by chronic high blood glucose (hyperglycaemia) and disturbance in the metabolism of carbohydrates, protein and fats. The hyperglycaemia is caused by either defects in insulin production or insensitivity to insulin, or both. (WHO, 1999) In type 1 diabetes, the destruction of the insulin-producing beta cells is usually an autoimmune process in people with a genetic susceptibility. The trigger for type 1 diabetes is not fully understood; many things are thought to be precursors, such as a coxsackie B4 virus or rubella.
3. Over time, hyperglycaemia damages the basement cell membrane of the blood vessels, causing damage to organs – specifically the eyes, kidneys, and heart. Nerve damage (neuropathy) also occurs and has many effects including sexual functioning, loss or impaired sensation in hands and feet, gastric emptying, and heart functioning. Metabolic control that results in blood glucose and blood pressure at target levels has been shown to reduce the risk for complications.
4. In 2010, it was estimated that over 300 million people worldwide were affected by diabetes. Within 20 years this number is expected to soar to about 500 million. This is an increase of more than 50%. Much of this increase will occur in the Indian and Asian subcontinents, due to a complex interplay of genetic, environmental and social factors, such as rural-urban migration and industrialisation. International Diabetes Federation. (2009). IDF Diabetes Atlas, 4th Ed. Brussels.
5. Although type 1 diabetes can occur at any time, diagnosis often occurs in childhood, especially during adolescence. Daily doses of exogenous insulin is required due to insufficient production of insulin by the pancreas. Recent epidemiological studies indicate increasing prevalence of type 1 diabetes in the under-five-years age group. Latent Autoimmune Diabetes in Adults (LADA) is the name applied to people diagnosed with diabetes as adults who are often not overweight and have little or no insensitivity to insulin. When special laboratory tests are done, people with LADA are found to have antibodies – especially GAD65 antibodies – that attack their beta cells. About 15% to 20% of people diagnosed with type 2 diabetes in fact have LADA. Most of type 1 diabetes is autoimmune, some is said to be idiopathic but the exact cause is not known. Type 2 diabetes accounts for about 90% of all people with diabetes. Gestational diabetes is hyperglycaemia with onset or first recognition during pregnancy. Symptoms of gestational diabetes are similar to Type 2 diabetes. Gestational diabetes is most often diagnosed through prenatal screening, rather than reported symptoms. (WHO, Diabetes Fact sheet N°312, November 2009)
6. The other specific types of diabetes are relatively rare. There are underlying pathology needs to be considered when deciding on management strategies. Maturity Onset Diabetes of the Young (MODY) (usually under 25) refers to a number of rare hereditary forms of diabetes due to defects of insulin secretion with minimal defects in insulin action Inherited defects in the action of insulin Diseases of the pancreas include cancer, cystic fibrosis, pancreatitis, and haemochromatosis Endocrine disorders – diseases associated with hormones that are antagonistic to insulin such as TSH, cortisol, glucagon, epinephrine, aldosterone etc) Some of these diseases are acromegally and Cushings syndrome Drug- or chemical-induced diabetes might arise from the use of medications such as steroids, diazoxide, thiazides or pentamadine, some chemotherapy and medications used to treat HIV/AIDS Infections associated with the development of diabetes include congenital rubella, coxsackie, citomegalovirus (CMV), and mumps Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2008). Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Can J Diab, 32(suppl 1).
7. Uncommon forms of immune-mediated diabetes – two known conditions: “Stiff-man” syndrome: an autoimmune disorder of the central nervous system characterised by stiffness of the axial muscles with painful spasms Anti-insulin receptor antibodies can cause diabetes by binding to the insulin receptor, blocking the action of insulin in target tissues. In some cases, these antibodies can act as an insulin agonist after binding to the receptor and can thereby cause hypoglycaemia (previously known as “type B insulin resistance”). A number of genetic syndromes are accompanied by an increased incidence of diabetes. These include Down’s syndrome, Turner syndrome, Prader Willi syndrome, Klinefelter, Wolfram and others. Gestational diabetes is fairly common depending on ethnic background. Estimates range from 3% to 7% of pregnant women. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Can J Diab 2008; 32(suppl 1).
8. The beta cells in the pancreas detect fluctuations in blood glucose and other nutrients. A rise in blood glucose results in the release of insulin from the Beta cells of the pancreas. The insulin helps to reduce blood glucose at three levels: muscle, fat and liver. Insulin acts to make the cell membrane receptive so that: Muscle tissue can take up glucose; any excess glucose is stored as glycogen Fat can take up glucose; any excess glucose is stored as fat In the liver, insulin stops the production of new glucose (gluconeogenesis), decreases the break-down of glycogen into dextrose (glycogenolysis), and promotes glycogen synthesis from glucose. Insulin also reduces the release of free fatty acids.
9. In type 1 diabetes, there is severe to total insulin deficiency. This results in the following: A decrease in glucose uptake by the muscle cells The breakdown of muscle into amino acids – then taken up by the liver and converted into new glucose (gluconeogenesis) An increase in the breakdown of triglycerides, leading to an increase in the release of free fatty acids – also taken up by the liver and converted into a usable energy form, ketones A reduction in the uptake of glucose by the liver and an increase in the breakdown of glycogen (glycogenolysis)
10. In about 95% of people with the condition, type 1 diabetes is an organ-specific autoimmune disease which results in pancreatic islet cell destruction. Evidence that type 1 diabetes is an autoimmune disorder is based on the presence, at the onset, of lymphocytic cells which infiltrate in and around the islets of the pancreas, as well as the occurrence of autoantibodies to islet-cell proteins ICA, IA-2, GAD (glutamic acid decarboxylase) and insulin autoantibodies. The progressive destruction of the beta cells is rapidly progressive in children and slowly progressive in adults (LADA – see slide 5). Preclinical diabetes refers to the months or years preceding the clinical presentation of type 1 diabetes, when islet antibodies can be detected as markers of beta-cell autoimmunity. In addition to these immunological markers, the risk of type 1 diabetes can further be determined by genetic markers. The parameters currently used to define the preclinical phase include: • Islet-cell autoantibodies • Glutamic acid decarboxylase autoantibodies (65K GAD isoform) • IA2 autoantibodies • Insulin autoantibodies • Special blood tests – human leukocyte antigen (HLA) typing Lawson, M., Muirhead, S.E., (2001). What is type 1 diabetes? In H. C. Gerstein & R.B. Haynes (Eds). Evidence-based Diabetes Care. Hamilton ON: BC Decker.
11. Genetic influences There is evidence that type 1 diabetes is, in part, a genetic disorder. Siblings of a person with type 1 diabetes are about 15 times more likely to develop diabetes than the general population. This translates into a risk of approximately 6% up to age 35 years. Interestingly, children in families with a mother with type 1 diabetes have a lower risk (~3%) than children in families with a father who has type 1 diabetes; the reasons for this are unknown. The genetic susceptibility is determined by the Histocompatibility leucocyte antigen (HLA) class II DR3/DR4, DQB non asp 57 and DQA arg 52 that increases the sensibility of the beta cell to damage by the autoimmune process triggered by environmental factors.   Identical (monozygotic) twins are more likely to both have type 1 diabetes than non-identical (dizygotic) twins. But concordance rates in identical twins are 25-50%, supporting the hypothesis that environmental factors are also important in the development of type 1 diabetes. Environmental factors The epidemiological patterns of type 1 diabetes, including geographic, seasonal, and temporal variations in incidence suggest that viruses may be important risk factors. Viruses are thought to act as initiators, accelerators or precipitators of the disease. These may attack and destroy the beta cells of the pancreas and directly cause diabetes. While multiple viruses appear to be associated with type 1 diabetes, most infected people never develop the disease. It is therefore unlikely that specific antiviral vaccines would significantly reduce the burden of type 1 diabetes in a community. The one proven environmental trigger of type 1 diabetes is congenital rubella. Other potential environmental triggers are enteroviral infections (particularly coxsackie B4), enteric cytopathic human orphan (ECHO) viruses (a group of enteroviruses that produce varying symptoms including rashes, respiratory illness, croup-like syndromes, and non specific fevers), casein, cow’s milk protein and gluten. Other autoimmune diseases are associated with type 1 diabetes such as Graves disease, thyroiditis of Hashimoto, Addison disease, vitiligo and pernicious anemia. American Diabetes Association. (2008). Medical management of type 1 diabetes, 5th ed. Alexandria VA: American Diabetes Association.
12. This slide shows the relationship between the genetic, environmental and immunological factors. As already discussed, people who develop type 1 diabetes have a genetic predisposition and are exposed to an environmental trigger. To develop type 1 diabetes, these people must have an abnormal immune response, thereby developing the antibodies that damage their beta cells. A progressive loss of beta cells occurs. As a result, the amount of insulin released decreases over a period of time. Symptoms of diabetes are present when endogenous insulin production is unable to meet the body’s requirements. In some people with newly diagnosed diabetes, treatment with insulin results in improved insulin secretion from the remaining small number of active beta-cells. The requirements of these people for injected insulin are therefore reduced temporarily. This is known as the “honeymoon” period and may last up to one year or longer. It is important to stress that the immunological destruction of beta cells continues and that after five to 10 years most people with type 1 diabetes have no endogenous insulin. American Diabetes Association. (2008). Medical management of type 1 diabetes, 5th ed. Alexandria VA: American Diabetes Association.
13. About 5% of people with type 1 diabetes have non-autoimmune type 1 diabetes. This type of diabetes is more common in African and Asian people. They are prone to ketoacidosis. However, none of the usual autoimmune markers discussed previously are present and there is no correlation with a type of HLA.
14. The incidence of type 1 diabetes is thought to be increasing. There is some geographic variation in the prevalence of type 1 diabetes. Finland reports the highest incidence (cases per 100 000 people per year) of type 1 diabetes (45.0) and Singapore one of the lowest (2.0). Type 1 diabetes occurs in all populations and across the socio-economic spectrum. Lawson, M., Muirhead, S.E. (2001). What is type 1 diabetes? In H. C. Gerstein & R.B. Haynes (Eds). Evidence-based Diabetes Care. Hamilton ON: BC Decker.
15. The peaks around pre-school possibly due to infections and puberty (11 to 12 years) possibly due to hormonal changes resulting in increased insulin requirements.
16. Type 2 diabetes is the most common form of diabetes – 90% to 95% of people with the condition. Unlike type 1 diabetes, people with type 2 diabetes still have some insulin production. Indeed, they may have higher blood levels of insulin than their counterparts without diabetes – albeit in response to higher-than-usual blood glucose concentrations. However, it is now understood that type 2 diabetes occurs with beta-cell loss. Excess body fat – particularly abdominal or visceral adiposity – is thought to contribute to the insulin insensitivity that is characteristic of this type of diabetes. It has been shown that people who carry excess weight around their abdomen are at higher risk of diabetes. Type 2 diabetes tends to develop slowly such that the symptoms of this condition, and therefore, the diagnosis, are often missed. Longstanding undetected hyperglycaemia – as often precedes the diagnosis of type 2 diabetes – may lead to the development of long-term diabetes complications. The United Kingdom Prospective Diabetes Study Group (UKPDS) demonstrated that more than 50% of people had complications when they were diagnosed. UK Prospective Diabetes Study Group. (1998). Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. Lancet, 352: 837-53.
17. Some 80% of people with type 2 diabetes have insensitivity to insulin. This means that they require significantly more circulating insulin in order to lower their blood glucose levels. People with type 2 diabetes therefore have a relative – rather than total – insulin deficiency. This results in reduced glucose uptake from muscle tissue and the liver. The breakdown of protein can occur in type 2 diabetes, but is significantly less pronounced than in type 1 diabetes. The liver contributes to the hyperglycaemia seen in people with type 2 diabetes by breaking down and releasing stored glucose (glycolysis) and, to a lesser extent, making new glucose (gluconeogenesis). Some of the excess glucose is taken up by the fat cells ...or taken up by the liver and converted to triglycerides. The storage of these triglycerides in the liver leads to hypertriglyceridemia and the “fatty liver” associated with insulin insensitivity.
18. Insulin does more than just work at the peripheral cell level. In the liver, insulin promotes the storage of glucose by inhibiting gluconeogenesis (the production of glucose from amino and fatty acids.) Insulin slows the production of glucose form glycogen (glycogenolysis) Insulin promotes the storage of glucose, by promoting the synthesis of glycogen from glucose. Insulin also promotes storage of glucose in the fat cells. Childs, B., Cypress, M., Spollett, G. (2005). Complete nurse’s guide to diabetes. Alexandria VA:American Diabetes Association.
19. There are multiple genes associated with type 2 diabetes. Some people with the condition may have a single gene defect, while others have multiple gene defects. This may explain why some people’s diabetes is easier to treat than others. In the early stages of insulin insensitivity, the pancreas produces more insulin than usual in an effort to overcome the insensitivity. Levels of insulin in the blood become excessively high (hyperinsulinaemia). Eventually the beta cells become “exhausted” and the amount of insulin produced decreases. Some recent studies have shown that poor foetal nutrition may cause a decrease in beta-cell formation, provoking diabetes in later life. Poor foetal nutrition is marked by low birth weight followed by rapid growth – with sufficient nutrition – within the first 12 months of life. Gillman, M. Rifis-Shiman, S berkley, C. et al. (2003) Maternal gestational diabetes, birth weight and adolescent obesity. Pediatrics, 111(3),e221-226. Exposure to high glucose levels in utero pre programs the foetus to poor glucose intolerance and diabetes later in life. Gillman, M., Rifis-Shiman, S.,Berkey, C et al. (2003). Maternal Gestational diabetes, Birth Weight and Adolescent Obesity. Pediatrics, 111, (3), e221-e226 The “thrifty gene” theory hypothesises that humans are genetically programmed to survive periods of famine. However, in times of abundance, particularly in the context of sedentary lifestyles and high-energy diets, these genes contribute to the excessive accumulation of fatty tissue, leading to insulin insensitivity and diabetes. There is a natural loss of beta-cell function as we age.
20. This slide shows the natural history of type 2 diabetes: The pale blue line represents insulin resistance – notice that it continues to increase as time goes on. Note the pale yellow line in this slide showing that approximately 50% of the beta cells are lost by the time a person is diagnosed with type 2 diabetes. The darker yellow line shows decreasing amounts of insulin released as Beta cells decrease. The dark blue line shows the fasting glucose rises as the number of Beta cells decrease, and the green line shows pot meal glucose rising over time as well. Note that post meal glucose rises before the fasting glucose does in the presences of decreasing amounts of insulin. It is also important to point out that complications start before the diagnosis is made as represented by the two bars at the bottom of the graph. The important message here is understanding of the process should encourage the appropriate use blood glucose lowering medicines. For many medicine will be necessary at the time of diagnosis. Slide courtesy of CADRE
21. The number of people affected by diabetes is increasing dramatically. This is thought to be due to a complex interplay of genetic, environmental and social factors. The prevalence of type 2 diabetes increases with age. Excess weight – abdominal fat in particular – increases insulin requirements and compounds the problem of insensitivity to insulin. Therefore, disturbing increases in the prevalence of type 2 diabetes reflect the rising prevalence of obesity. Globalization and urbanization are changing lifestyle choices resulting in less physical activity and more calorie dense foods. Research has shown that some ethnic groups are at higher risk than others. Communities of Asian Indians and people from African origin, for example, show higher rates of type 2 diabetes and appear to suffer more in terms of diabetes complications – such as kidney failure – compared to Caucasian populations. The greatest increase in prevalence is found in low and middle income countries and the African Region has the highest increase in prevalence at 98%. There are particularly disturbing trends in adolescents – thought to be exacerbated by decreased exercise and increased calorie and fat intake. There is an increase in prevalence found in children and adolescents worldwide with geographic differences in trends. Data from the US in 2000 reported a 10 to 30 fold increase in the number of children with type 2 diabetes over 10-15 years. There is concern that these young people will develop complications earlier in their life which will have ramifications for individuals, families and the health care system. Fagot-Campagna, A. (2000). Emergence of type 2 diabetes in children: epidemiological evidence. J Pediatr Endocrinol Metab, 13(suppl 6), 1395 1402. International Diabetes Federation. (2009). IDF Diabetes Atlas, 4th Ed. Brussels.
22. Note to the educator: Give participants time to reflect on the question individually and/or in pairs before opening the discussion up to the whole group. The following slide provides a list of risk factors.
23. There are many risk factors for type 2 diabetes. Some are preventable and a great deal of work has been done to try to develop programmes to prevent diabetes. We will look at this work later in this module. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2008). Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Can J Diab, 32(suppl 1).
24. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2008). Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Can J Diab, 32(suppl 1).
25. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2008). Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Can J Diab, 32(suppl 1).
26. The signs and symptoms of type 2 diabetes are often missed by people and their healthcare professionals. Many are also signs of ageing such as fatigue, weight loss, nocturia, etc. (WHO, Diabetes, Fact sheet N°312, November 2009)
27. Note: values for venous plasma samples Note: ** confirmation of the diagnosis depends on repeated values done on another day, unless unequivocal hyperglycaemia and metabolic decompensation are present. IFG and IGT are often referred to as “prediabetes” or “people at risk”. These people are at increased risk for cardiovascular disease and development of diabetes, they should be targeted for prevention strategies. Diagnosis based on A1C was recommended by a US consensus panel in 2010. It has not yet been accepted worldwide partly because of the different standards in laboratory testing. ADA. (2010). American Diabetes Association Position Statement Diagnosis and Classification of Diabetes Mellitus. Diabetes Care, 33: S62-69. World Health Organization. (2006). Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia. Geneva: WHO Document Production Services.
28. Impaired glucose tolerance is commonly referred to as “IGT”; impaired fasting glucose as “IFG”. IGT and IFG are intermediate conditions that reflect a change in the physiological response to glucose. This change represents a transitive state between a normal response and diabetes. People with IGT or IFG are at high risk of progressing to type 2 diabetes, although this is not inevitable. These two stages, often referred to as “prediabetes” or “people at risk”, should be recognised and managed in order to prevent or delay the onset of diabetes and to prevent or delay the onset of cardiovascular disease (CVD). IFG and IGT are considered risk factors for diabetes and for CVD. Data suggest that the prevalence of type 2 diabetes is only a small proportion of the overall prevalence of glucose intolerance. People with either undiagnosed type 2 diabetes or IGT are thought to be far more numerous than the diagnosed population with type 2 diabetes. This is especially the case in older people (above 65 years), of whom about two-fifths may have IGT or undiagnosed type 2 diabetes. International Diabetes Federation. (2009). Diabetes Atlas, 4th ed. Brussels: IDF. ADA. (2010). American Diabetes Association Standards of Medical Care in Diabetes 2010. Diabetes Care, 33, S11-S61.
29. The oral glucose tolerance test (OGTT), consists of a 75 g glucose load taken in the morning after an 8-10 hour non-caloric fast. Water is allowed, but not tea or coffee. In preparation for the test people should be told not to smoke, not to take certain medications such as steroids and to eat their normal intake of carbohydrate each day for 3 days prior to the test. Venous blood glucose levels are taken in the fasting state and at 1 and 2 hours after drinking the glucose. If an OGTT is necessary it should be done under optimised, supervised conditions. Various factors might affect the reliability of the test: Avoidance of carbohydrate over several days reduces the first-phase insulin response to glucose. It also results in a delayed second-phase response, increasing the risk of a false positive OGTT result. Therefore, people should be asked to eat their normal carbohydrate load during the days leading up to the test Glucose tolerance changes throughout the 24-hour period Glucose tolerance is also affected by illness; therefore OGTT should be performed in the morning, only in people who are well People should rest throughout the test in a semi-reclined position and not breastfeed; both exercise and breastfeeding will increase glucose disposal (WHO, Lab Diagnosis and Monitoring of Diabetes, 2002)
30. Several tests can assist in a differential diagnosis of type 1 diabetes and type 2 diabetes when the diagnosis is unclear. The presence of ketones in the urine indicate insulin deficiency and point towards the diagnosis of type 1 diabetes but is not definitive. Likewise, the presence of the antibodies associated with beta-cell destruction (islet-cell antibodies/GAD antibodies) can be used for differential diagnosis. Insulin assays are unable to distinguish endogenous versus injected insulin. Pro-insulin, the precursor to endogenous insulin, is formed by two circular chains of peptides. On release, pro-insulin is cleaved into the insulin protein and C-peptide chain. Decreased C-peptide is used as a marker of reduced endogenous insulin production and points to a diagnosis of type 1 diabetes. In a person with type 2 diabetes it shows that insulin would be the appropriate treatment. (WHO, Lab Diagnosis and Monitoring of Diabetes, 2002)
31. The metabolic syndrome is a cluster of risk factors: Impaired glucose metabolism Central obesity Dyslipidaemia Hypertension While the metabolic syndrome is found in 70% to 80% of people with type 2 diabetes, it affects fewer than one in four of those with normal blood glucose levels. There is still some controversy as to whether the metabolic syndrome is a true syndrome or a cluster of risk factors. There is also varying diagnostic criteria around the world: National Cholesterol Education Program Adult Treatment Panel III (ATP III), WHO, and recently IDF. The IDF definition highlights waist circumference as the key risk indicator and includes ethnicity-specific cut-off points for obesity. The more components of the syndrome people have, the higher their risk. In one study from Scandinavia, cardiovascular deaths occurred in 12% of those with the metabolic syndrome, but in only 2% of those without the syndrome. These risk factors combine to double the risk of coronary heart disease and stroke. Deaths from cardiovascular disease are also increased, emphasizing the need to treat these risk factors aggressively. International Diabetes Federation. (2006). The IDF Consensus worldwide definition of the metabolic syndrome. Brussels: IDF.
32. Although a cure for type 1 diabetes is not currently available, clinical trials have been undertaken to evaluate a variety of approaches for primary prevention. None to date have shown that type 1 diabetes can be prevented.
33. Several recent trials have demonstrated that type 2 diabetes can be delayed or prevented at least in the short term. The Da Qing study in China followed 577 people for six years. There were three groups: Those with a diet intervention Those with an exercise intervention Those with both diet and exercise The reductions in risk were as follows: 31% in the diet only group 46% in the exercise only group 41% in the diet and exercise group. The Finnish Diabetes Prevention Study, which involved 522 people, had two groups: a control group a group who had a diet and exercise intervention. They were followed for 3.2 years. All people in the study had IGT. It was found that the group with the diet-and-exercise intervention had a 58% decreased incidence of type 2 diabetes. Pan, X,. Li, G., Hu, Y., et al. (1997). Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care, 20(4): 537-44. Tuomilehto J, Lindstrom J, Eriksson JG, et al. (2001). Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Eng J Med, 344: 1343-50.
34. In the Diabetes Prevention Program, all the 3234 people involved had IGT. There were three groups: Control Metformin Diet and exercise The groups were followed for 2.8 years. The risk reductions were as follows: 31% in the metformin group 58% in the diet and exercise group – the same as in the Finnish study The Study to Prevent Non Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) used an alpha glucosidase inhibitor, acarbose, in an attempt to reduce the incidence of type 2 diabetes. 1368 people were followed for 3.3 years; a significant reduction (20%) in the incidence of type 2 diabetes was demonstrated. We now know that type 2 diabetes can be delayed in people who have IGT. Work needs to be done at community levels to reduce obesity by increasing opportunities for (and perceived value in) increased physical activity, while at the same time reducing people’s caloric and fat intake. A number of countries have national initiatives in place to help people eat less and walk more. In the Diabetes Reduction Assesment with Rampiril and Rosiglitazone Medication (DREAM) study 5269 people with either IGT or IFG were randomised to groups using ramipril or placebo or rosiglitazone (a TZD) or placebo and followed for 3 years. Diabetes or death was reduced by 60% in those randomised to the TZD compared with placebo. The reduction in the group using ramipril was not significant. In the XENical in the Prevention of Diabetes in Obese Subjects (XENDOS) study 3305 patients (79% normal glucose tolerance, 21% with IGT) were randomised to lifestyle plus either orlistat 3x daily or placebo. Patients had a BMI > 30 kg/m2 After 4 years the cumulative incidence of diabetes was 9% in the placebo group and 6.2% in the orlistat group corresponding to a risk reduction of 37.3%. Reduction in diabetes was evident only in those with IGT. Chiasson, J.L., Josse, R.G., Gomis, R., et al. (2002). Acarbose for prevention of type 2 diabetes mellitus: The STOP-NIDDM randomized trial. Lancet, 346, 393-403. DREAM (Diabetes REduction Assessment with ramipril and rosiglitazone Medication) Trial. (2006). Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial. Lancet, 368(9541), 1096-105. The Diabetes Prevention Program Research Group. (2002). The diabetes prevention Program (DPP). Diabetes Care, 23(12), 2165-71. Torgerson, J.S., Hauptman, J., Boldrin, M.N., Sjostrom, L. (2004). XENical in the prevention of diabetes in obese subjects (XENDOS) Study. Diabetes Care, 27(1), 155-161.
35. Note to educator: Give participants time to reflect on the question individually and/or in pairs before pooling ideas and suggestions from the group.