Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Beware of the carbs!
- Uffe Ravnskov (8 December 2006)
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HbA1c: Time for a change in a very confusing scale.
- Alain Braillon (9 December 2006)
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Management of hyperglycaemia in type 2 diabetes: Licensed indications for existing oral hypoglycaemic therapy in the United Kingdom
- John R Lindsay, Belfast, UK, BT9 7AB (10 December 2006)
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Overegging the pudding.
- David Leopold (10 December 2006)
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It's not just science, but also common sense, that supports the use of low-carb diets in the management of diabetes
- John P Briffa (10 December 2006)
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"Sugar Disease"
- Melchior Meijer (12 December 2006)
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Prevent diabetes, don't treat symptoms
- Barry A Groves, PhD (13 December 2006)
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Glycaemic control in type 2 diabetic patients and hemorheologic parameters
- Larisa I Carrera, Raúl G Etchepare, Mabel D´Arrigo, Stella M Vaira, Juana Valverde, Patricia Foresto, Alberto E D'Ottavio (14 December 2006)
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Role of anti obesity pills in hyperglycaemia
- Babulayeb Mukhopadhyay (15 December 2006)
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Drugs for T2DM: the new are still unproven.
- Neil D Burman (27 December 2006)
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Lifestyle changes have great potential in the prevention and treatment of type 2 diabetes
- Matti Uusitupa, Jaana Lindström, Markku Peltonen, and Jaakko Tuomilehto (29 December 2006)
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Uffe Ravnskov, independent researcher Magle Stora Kyrkogata 9, 22350 Lund, Sweden
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In their review Heine and colleagues claim that there are “no high quality data to support the effectiveness of dietary treatment of type 2 diabetes” referring to a recent Cochrane analysis.1 However, at least 22 experiments have documented the benefits of reducing the dietary intake of carbohydrates in type 2 diabetics.2-23 Most of them were controlled studies where a low- carbohydrate diet was compared with a low-fat diet, and almost all of them found that the former was better than the latter as regards weight reduction and glycemic control. In several of the low- carbohydrate groups patients were even able to reduce or stop their antidiabetic treatment. Most of these studies were ignored by the Cochrane authors because their length was shorter than six months. However, to-day four studies with a length of six months or longer have been published and with similar benefits as in the short-term experiments.14, 15, 19, 23 The main argument against a low-carbohydrate diet is that we do not know the long-term effects. Concern has in particular been raised about an increased risk of cardiovascular disease because of the higher intake of dietary fat, and an increased risk of renal failure because of the higher intake of protein. The first argument is invalid because in almost all studies total and LDL-cholesterol were unchanged, in a few HDL cholesterol went up and in almost all studies the low-carbohydrate diet was followed by a significant reduction of the triglycerides. The second argument is based on the finding that a reduction of dietary protein may retard the development of renal failure in patients with kidney disase indirectly suggesting that a high intake may have the opposite effect. There is no evidence that a high protein intake may worsen renal function in healthy people,24 but the high incidence of nephropathy in type 2 diabetes is reason for concern in this aspect However, the other benefits from the low-carbohydrate diet may probably outweigh this risk because in a recent case report it was possible to reverse a steady worsening of the renal function in a patient with diabetic nephropathy by reducing his intake of carbohydrates.25 The resistence against the
low-carbohydrate diet is particularly curious in view of the fact
that no long-term trial has ever shown that a low-fat diet is effective
in diabetic patients or in other people, neither for improving glycemic control
or for reducing the risk of cardiovascular disease. References
, Competing interests: None declared |
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Alain Braillon, Public Health Department University hospitals. 80000 Amiens, France.
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Heine et al propose several important measures to improve glycemic control, a major problem which looks like the Grail.1 However, acting on the misrepresentation of the importance of changes in HbA1c is a missing point « Small » absolute change such as a 1% reduction in HbA1c is associated with reductions in risk of 21% for deaths related to diabetes and 37% for microvascular complications.2 However, the patient’s misrepresentation of the importance of changes in HbA1c has been demonstrated by changing the scale of the results.3 We think a new scale for HbA1c could improve the concern of both patients and physicians for metabolic control: John would be more concerned by a change from 790 IU to 750 UI than from 7,9% to 7,5% (0.4% absolute change). More complex mathematical transformations may be even more stimulating References 1. Heine R J, Diamant M, Mbanya JC, Nathan DM. Management of hyperglycaemia in type 2 diabetes: the end of recurrent failure? BMJ 2006;333:1200-1204 2. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;321:405–412. 3. Hanas R. Psychological impact of changing the scale of reported HbA(1c) results affects metabolic control. Diabetes Care. 2002;25:2110-1. Competing interests: None declared |
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John R Lindsay, Specialist Registrar Belfast City Hospital, Belfast, UK, BT9 7AB
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Editor The recent article by Heine et al. on the management of hyperglycaemia in type 2 diabetes provides a helpful clinical review of existing pharmacological strategies (1). The authors’ rightly suggest that the meglitinide and alpha- glucosidase inhibitors drug classes are less widely prescribed presumably because of lack of efficacy, cost, multiple daily dosing or due to gastrointestinal side-effects (1). However, I wish to draw attention to inaccuracies within Table 1 regarding licensed indications for existing oral hypoglycaemic agents in the United Kingdom. The British National Formulary clearly states that alpha-glucosidase inhibitors and meglitinides are licensed for management of type 2 diabetes in the UK (2). In the case of acarbose, the drug may be used for patients inadequately controlled by diet or by diet with oral antidiabetic drugs (2). The meglitinides, nateglinide and repaglinide, are also licensed in the UK for treatment of type 2 diabetes. The former may be used in combination with metformin, whereas the latter is licensed as monotherapy or with metformin when metformin alone is inadequate (2). It is unclear whether the treatment algorithm in Figure 3 in respect of the timing of introduction of the thiazolidinedione drug class in type 2 diabetes will be altered by the results of the recently published ADOPT study (A Diabetes Outcome Progression Trial) (3). In this study the authors examine the efficacy of thiazolidindiones as compared with other glucose-lowering medications in maintaining long-term glycaemic control in type 2 diabetes. Cumulative incidences of failure with monotherapy at 5 years were 15% with rosiglitazone, 21% with metformin and 34% with glibenclamide for patients with recently diagnosed type 2 diabetes. An accompanying Editorial in the New England Journal of Medicine by Dr Nathan suggests that metformin will remain the first option when commencing pharmacological therapy. I support this assertion; I also concur that ultimately the choice between the glitazones and sulphonylurea drug classes for add on therapy will depend on ‘the relative costs of these medications, their profiles of adverse events, and their potential risks and benefits’ (4). 1. Heine RJ, Diamant M, Mbanya JC, Nathan DM. Management of Hyperglycaemia in type 2 diabetes. British Medical Journal 2006;333:1200- 4. 2. Joint Formulary Committee. British National Formulary. 51 ed. London: British Medical Association and Royal Pharmaceutical Society of Great Britain; 2006. 3. Kahn SE, Haffner SM, Heise MA, Herman WH, Holman RR, Jones NP, et al. Glycemic Durability of Rosiglitazone, Metformin, or Glyburide Monotherapy. N Engl J Med 2006;355(23):2427-2443. 4. Nathan DM. Thiazolidinediones for Initial Treatment of Type 2 Diabetes? N Engl J Med 2006;355(23):2477-2480. Competing interests: None declared |
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David Leopold, Physician Swansea SA4 4JE
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Dear Sir. The focus upon glycaemic control which once dominated management of T2 diabetes has been tempered since the relatively overwhelming effectiveness of antihypertensive treatment has been more widely accepted. In primary insulin-deficiency (T1) it is both logical and well- established that accurate insulin replacement is effective, ..it is worrying that this is quoted in a discussion of the wholly different condition of primary insulin resistance..T2. Although the breathless enthusiasm of the reviewers makes it hard to be sure, would it be fair to say the only reliable information about the outcomes produced by various treatments for T2 comes from the UKPDS..? The UKPDS results clearly show that attempts to improve outcome thro' intensive glycaemic control are ineffective.: With intensive glycaemic control HgA1C could be reduced from 7.9% to 7.0%....but.. This had no significant effect on diabetes-related deaths, nor on all- cause mortality, nor on vascular diseases. In fact, the best outcomes in UKPDS were associated with use of metformin, but its slight effect on HbA1c suggests this had little or nothing to do with glycaemic control. It would help debate if the authors could clarify any support for their enthusiasm from outcome data, and explain why, in their conclusion, they conflate antihypertensive treatment (uncontroversial), when their paper was about glycaemic treatment(Contentious)? The issue is of much more than academic interest, since there is a vast potential market for glycaemic agents, and much NHS resource is already consumed in attempts at glycaemic control... 1.McCormack J, Greenhalgh T. Seeing what you want to see in randomised controlled trials: versions and perversions of UKPDS data. BMJ 2000;320:1720-1723. 2.UKPDS Group. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes Lancet 1998;352:837-853. Yours faithfully David Leopold Competing interests: None declared |
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John P Briffa, Doctor and writer Woolaston House, 25 Southwood Lane, Highgate, London N6 5ED
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In reference to Heine and colleagues’ article on the management of type 2 diabetes [1] Uffe Ravnskov summarises the research which supports the use of low-carbohydrate diets in this respect [2]. Much of this research focuses on the use of diets which have low ‘glycaemic index’ (GI). The GI is essentially a measure of the extent of sugar release from a food. It is noteworthy that in a meta-analysis of intervention studies comparing low- and high-GI diets, the lower-GI approach was, overall, found to reduce HbA1c levels by 0.43 per cent points [3]. Perhaps an even more useful measure of the influence of diet on glycaemia is what is known as the glycaemic load (GL) – calculated by multiplying the GI by the amount of carbohydrate found in a standard portion of food. Starchy carbohydrates such as bread, potatoes rice, pasta and breakfast cereals turn out to have generally high glycaemic load [4]. Yet, it is these very same foods that diabetics are usually encouraged to have their fill of. For instance, the website of Diabetes UK, the UK’s leading diabetes charity, advises individuals to include starchy carbohydrates at each meal [5]. In reference to this, the site adds: “The amount of carbohydrate you eat is important to control your blood glucose levels”. The cryptic message here seems to be that diabetics somehow require starchy carbohydrates to maintain blood sugar control. But does logic not dictate that the less carbohydrate one eats, the less disruption there will be in blood glucose levels? Starchy carbohydrates have been proven to have high GIs and the more we eat of them, the greater the resultant glycaemia. Should we really be encouraging individuals who have a fundamental problem with blood sugar control to emphasise in the diet foods known to have considerable capacity to raise blood sugar levels?! There is plenty of science which supports the use of low-carb/GI/GL diets in the management of diabetes. But forget the science for a moment – another reason why this approach has obvious merit relates to the fact that it is based on common sense. References: 1. R J Heine, et al. Management of hyperglycaemia in type 2 diabetes: the end of recurrent failure? BMJ 2006;333:1200-4 2. Ravnsov U. Beware of the carbs! BMJ 8th December 2006 (rapid response) 3. Brand-Miller J, et al. Low–glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care 26:2261–2267, 2003 4. Kaye Foster-Powell, et al. Susanna International table of glycemic index and glycemic load values: 2002 Am J Clin Nutr 2002;76:5-56. 5. www.diabetes.org.uk Contact: john@drbriffa.com http://www.drbriffa.com Competing interests: None declared |
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Melchior Meijer, Medical Writer Meijer & Konow 9974 RR Zoutkamp (Netherlands)
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The Dutch call diabetes simply 'suikerziekte' meaning 'sugar disease', a condition defined by high blood sugar levels. Glucose in the mouth, glucose out in the blood stream. Shouldn't all control of diabetes start by focusing on the type and amount of blood sugar triggering foods? "The [lifestyle and multiple drug] algorithm described here will probably not slow down the clinical outcome of type 2 diabetes," bluntly conclude Heine et al (1). The low(2) or 'slow' carb intake approach is not part of their algorithm; it should be, we're talking 'suikerziekte'. melchior.meijer{at}planet.nl 1. R J Heine, et al. Management of hyperglycaemia in type 2 diabetes:the end of recurrent failure? BMJ 2006;333:1200-4 2. Nielsen JV, Joensson E. Low-carbohydrate diet in type 2 diabetes. Stable improvement of bodyweight and glycemic control during 22 months follow-up. Nutr Metab (Lond). 2006 Jun 14;3:22. Medline 16774674 http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-22.pdf Competing interests: None declared |
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Barry A Groves, PhD, Independent Researcher, maintains www.second-opinions.co.uk OX7 6LP
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I was disappointed with Heine, et al's paper because it contained nothing whatever to help diabetics. The reason for the "recurrent failure" is that the population is advised to consume a dietary regime that causes diabetes and when the disease becomes apparent, only the symptoms are treated with drugs. Reliance on drugs will never cure the disease; they actually worsen the prognosis. It is no secret that diabetes is a disease of carbohydrate metabolism. We have known since 1935 that excess carbs are the cause of Type-2 diabetes;[1] and more recent studies have shown that reducing dietary carbs cures existing diabetes and prevents its occurrence. In my experience, Type-2 diabetes is the easiest condition to prevent; and it can be totally cured in as little as one day. Despite this wealth of evidence, diabetics are still told by their trained(?) advisers to eat foods that will raise their serum glucose levels and are then prescribed drugs to reduce those levels to prevent complications. Can someone please explain to me where the sense is in that? Why are patients not advised to reduce their intakes of foods rich in cereals and/or sugars (including fruit)? Incidentally, such a dietary strategy has also been shown to benefit or even cure Type-1.[2] Beta cells in Type-1 diabetics can regenerate even after 60 years from first diagnosis.[3] If the pancreas is relieved of the constant pressure to lower excessive glucose levels from incorrect diet, it can often cope so well with the low glucose levels found on a low-carb, high-fat diet, that insulin injection can be discontinued. References 1. Given H D C. A New Angle on Health. John Bale, Sons & Danielsson Ltd. 1935. 2. Kwasniewski. J, Chylinski M. Homo Optimus. Wydawnictwo WGP, Warsaw, 2000: 163-6. 3. Butler PC. Beta-Cells Regenerate Even In Type 1 Diabetes. ADA 57th Scientific Sessions, June 2005. Competing interests: None declared |
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Larisa I Carrera, Medical Professor and Researcher Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Argentina, Raúl G Etchepare, Mabel D´Arrigo, Stella M Vaira, Juana Valverde, Patricia Foresto, Alberto E D'Ottavio
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The hemorheologic parameters need to be considered for evaluating patients affected by type 2 diabetes because those variables contribute to the development of their microangiopathy and ensuing complications (1, 2). In this regard, recovering still unpublished preliminary results ethically obtained in 25 diabetic patients (13 with microangiopathic skin lesions and 12 without) and in 25 healthy controls, we characterized two models using a linear discriminant analysis to determine which variables discriminate between two or more naturally occurring groups (3):(a) Discriminant function in Model 1 = 0.55 Aggregate Shape Parameter (ASP) – 0.60 Whole Blood Viscosity (WB Visc) 230 + 0.83 serum fibrinogen when discriminating healthy individuals from diabetic patients with skin lesions, and (b) Discriminant function in Model 2 = 6.303 ASP – 0.339 WB Visc 230 + 0.010 serum fibrinogen when discriminating healthy controls from diabetic patients with and without skin lesions. Both models were validated through the coefficient of canonic correlation, the Mahalanobis distance, the percentage of classification and the centroids of each group(Model 1: 0,920, P < 10-3, 100%, 0.90 and 5.59, respectively; Model 2: 0,890, P < 10-3, 86 %, -1.7, 1.7 and 2.2, respectively).In line with the relevance of managing hyperglycaemia in type 2 diabetes according to Heine et al., some authors reported an improvement in some hemorheologic parameters when a strict glycaemic control was carried out in type 2 diabetic patients (4). Furthermore, we estimate that both models here characterized may be also helpful for their biochemical monitoring. 1. Le Devehat C, Vimeux M, Khodabandehlou T: Blood rheology in patients with diabetes mellitus. Clinical Hemorheology and Microcirculation 2004; 30: 297-300 2. Marton Z, Kesmarky G, Vekasi J, Cser A, Russai R, Horbath B, Toth K: Red blood cell aggregation measurements in whole blood and in fibrinogen solutions by different methods. Clinical Hemorheology and Microcirculation 2001; 24: 75-83. 3. Altman D: Practical Statistics for medical Research Ed. Chapman & Hall. London (UK), 1997 4. Babu N, Singh M: Influence of hyperglycemia on aggregation, deformability and shape parameters of erythrocytes. Clinical Hemorheology and Microcirculation 2004; 31: 273-80 Competing interests: None declared |
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Babulayeb Mukhopadhyay, Consultant Endocrinologist Hairmyres Hospital, Scotland, G75 8RG
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I am slightly surprised to see that Heine and colleagues have not mentioned the evidence of anti obesity agents in diabetes. As more than 80% of patients with type 2 diabetes are overweight or obese at presentation,and most patients gain weight over a period of time on oral therapy, agents that promote weight loss should be considered. There is now good evidence that Rimonabant, a CB 1 receptor antagonist, can induce weight loss and reduce HbA1c by 0.6% in type 2 diabetes (RIO - Diabetes Study, Lancet, 2006). Similar results are avialable for Orlistat. One would be inclined to think that such agents should have a role in management of obese type 2 diabetes patients unable to lose weight on metformin alone. Competing interests: None declared |
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Neil D Burman, Preventative Internist HealthSpan Research, Cape Town
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The type 2 diabetes T2DM review by Heine, Nathan et as has notable omissions: Prevention comes before treatment. Overweight (adult BMI above 23kg/sqm, or body fat mass above about 15kg) precedes type 2 diabetes T2DM by years. Few folk achieve the right balance of exercise, lean mass and fat mass. In the non-obese, BMI is a poor guide to adiposity - and in all long term studies (USA, UK, Dutch), future risk rises relentlessly with youthful BMI above 22kg/sqm. Metformin is the only proven drug which – titrated to tolerance - stops or reverses lipidemia, thrombotic disease, insulin resistance, and weight gain (metformin lowers obesity by about 8% - eg Glueck 2006). The 20year UKPDS 1998 showed that metformin was associated with no weight increase, and (as in the 5year Saskatchewan diabetic health database –Johnson 2002) reduction in all-cause mortality including cancer by almost 40%. Modest doses of metformin for 3-4years in diabetes prevention studies (USA -DPPRG 2002, India -Ramachandran 2006 and China- Y Wenying 2001) lowered incidence of new diabetes respectively by 31%, 33% and 70%. No other synthetic drug heavily used long term- in primary chronic prevention of all the major common degenerative diseases - safely achieves what metformin does – psychotropes, statins, sulphonylureas, glitazones, antihypertensives, oral sex hormones, nonsteroidal anti-inflammatories etc. Intolerance to metformin is always relative: start with eg ¼ tab/day, and build up slowly to just avoid nausea and diarrhoea. 3gm/day may be well tolerated. Before considering any newer anti-diabetic drugs - all of which have no proven long term safety record, and major hazards eg silent hypoglycemia, weight gain, cance, cardiovascular disease)- one should minimize other major iatrogenic risks eg diuretics, cortisone, psychotropes and oral sex hormones (OC, HT). Thus, consider low dose co-amiloretic and low dose reserpine for hypertension; 5-hydroxytryphan for depression; the Mirena for contraception; and appropriate physiological human sexhormone replacement with systemic testosterone, plus systemic estradiol for women. This requires simply that from “middle age”, and in the overweight from any age, a fasting sex hormone profile should be measured as routinely as glucose, insulin, blood pressure and body composition (height, weight, waist girth, and calculated if not measured body fat and lean mass). neil.burman@gmail.com Competing interests: None declared |
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Matti Uusitupa, Professor University of Kuopio, 70211 Kuopio, Finland, Jaana Lindström, Markku Peltonen, and Jaakko Tuomilehto
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EDITOR - In their clinical review on the management of hyperglycaemia in type 2 diabetes Heine et al (1) conclude that despite the demonstrated efficacy, evidence for the successful and durable lifestyle modification in diabetes is lacking. The view is based on a recent Cochrane analysis, but this approach may not be totally valid and fair to evaluate the impact of diet and other lifestyles in the treatment of type 2 diabetes. This is because lifestyle intervention trials are demanding to carry out due to the lack of expertise, enthusiasm and financial support. The common concern has been that it is much more difficult to get money for lifestyle interventions than for long-term drug trials financed by big pharmaceutical companies. The success of lifestyle modification is based on the changes achieved. If you are not able to change lifestyles of your patients you can not expect any major effects, either. We see that a Cochrane analysis or meta-analysis combining the data from lifestyle intervention studies carried out with quite different management strategies with regard to dietary and exercise counseling and follow-up measurements, may result in too pessimistic view in terms of long-term benefit of lifestyle changes in type 2 diabetes. It is of note that the expert group of the Diabetes and Nutrition Study Group of the EASD has recently given evidence-based nutritional approaches to the treatment and prevention of diabetes. These emphasise the key role of diet therapy not only with regard to the treatment and prevention of type 2 diabetes but also the prevention of atherosclerotic vascular complications (2). Now, we have strong evidence that type 2 diabetes is preventable by lifestyle changes (3). Even modest long-term weight reduction (with qualitative changes in diet and increased physical activity) improves insulin sensitivity in long-term and may halt the progressive decline in insulin secretion in persons with IGT (4). When it comes to the known risk factors and pathogenesis of type 2 diabetes, lifestyle changes are also “most specific” approach among various treatment modalities. We analysed the effect of lifestyle changes separately in two hyperglycaemic groups in the Finnish Diabetes Prevention Study (3). Lifestyle changes had a significant improvement in glycaemia irrespective of baseline 2-h glucose level at OGTT (Table). Furthermore, during the 7-year follow-up the risk of diabetes was similarly reduced in both intervention subgroups formed by median 2-h glucose value. This is in line with the results of our earlier controlled study with recently diagnosed type 2 diabetes; one year after a 12 months intensified lifestyle intervention the intervention group had 0.5 % unit lower HbA1c level than the control group did, and 55.3% in the intervention vs. 31.8% of the control patients had HbA1c under 7.0%, P=0.016. Furthermore, only 12.5% needed oral drugs in the intervention group vs. 34.8% in the control group, P=0.0059 (5). Weight reduction and healthy diet also modify different adipokines and inflammatory factors to the direction, which may halt the progression of type 2 diabetes. Treatment should be started as early as possible in the prediabetic phase, but lifestyles belong to the treatment of type 2 diabetes at its all phases. Finally, weight reduction, healthy diet and physical activity do not harm the diabetic patient as the newer drugs may do, since the long-term safety of these drugs remains unknown. We do agree with the authors than well-conducted lifestyle intervention studies are urgently needed, but they are not possible without financial support, multicentre approach and changes of our attitude as for how to value different treatment modalities. Matti Uusitupa
(1), Jaana Lindström (2), Markku Peltonen (2) and Jaakko Tuomilehto (3) 1 School of Public Health and Clinical Nutrition, Clinical
Nutrition, Correspondence: Matti Uusitupa matti.uusitupa{at}uku.fi 1. Heine RJ, Diamant M, Mbanya J-C, Nathan DM. Management of hyperglycaemia in type 2 diabetes. BMJ 2006;333;1200-04. 2. Mann JI, De Leeuw I, Hermansen K, Karamanos N, Riccardi G, Karlaström B et al. Evidence-based nutritional approaches to the treatment and prevention of diabetes mellitus. Nutr Metab Cardiovasc Dis 2004;14:373-94. 3. Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K et al. Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. Lancet 2006;368:1673-9. 4. Uusitupa M, Lindi V, Louheranta A, Salopuro T, Lindström J, Tuomilehto J for the Finnish Diabetes Prevention Study Group. Long-term improvement in insulin sensitivity by changing lifestyles of people with impaired glucose tolerance. 4-year results from the Finnish Diabetes Prevention Study. Diabetes 2003;52:2532-8. 5. Uusitupa M, Laitinen J, Siitonen O, Vanninen E, Pyörälä K. The maintenance of improved metabolic control after intensified diet therapy in recent type 2 diabetes. Diab Res Clin Pract 1993;19:227-38. Table. Changes in body weight, 2h glucose, and HbA1c from baseline to 1-year follow-up, and diabetes incidence by treatment group and baseline 2h glucose at baseline in the Finnish Diabetes Prevention Study (DPS).
Competing interests: None declared |
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